Causes of headaches

Possible causes of headache:

• infectious diseases of the central nervous system - meningitis, brain abscess, arachnoiditis, encephalitis, malaria, typhus (Brill's disease);
• non-infectious diseases of the central nervous system - brain tumors, subarachnoid hemorrhage, increased intracranial pressure, temporal arteritis, closed-angle glaucoma, trigeminal neuralgia, poisoning with medications or carbon monoxide, food poisoning;
• mental or psychological condition - neuroses, asthenic conditions after flu and other infectious diseases;
• other diseases such as arterial hypertension, anemia, thrombosis, sinusitis, middle ear diseases, contusion, trauma, etc.

Headache can be functional or organic. Organic headache will usually be associated with neurological symptoms and signs such as vomiting, fever, paralysis, paresis, seizures, confusion, decreased consciousness, mood changes, visual disturbances.

When searching for the causes of headaches, one must also take into account the patient's age.

Causes of chronic headaches in different age groups

Children (3 to 16 years old)	Adults (17 - 65 years)	Elderly (over 65 years old)
Migraine. Psychogenic pain. Tension pain. Post-traumatic. Tumors (rare, mainly of the brainstem and posterior cranial fossa)	Tension headache. Migraine. Post-traumatic. Cluster headache. Tumors. Chronic subdural hematoma. Cervicogenic. Glaucoma	Cervicogenic headache. Cranial arteritis. Persistent tension headache. Persistent migraine. Rarely cluster headache. Tumors. Chronic subdural hematoma. Glaucoma. Paget's disease (osteitis deformans)

Headache may occur with a variety of intracranial or extracranial diseases. Their rapid diagnosis and adequate therapy are often critical. Treatment of the underlying disease that causes secondary headaches has a positive effect on the headache itself. In general, a description of the treatment of secondary headaches is beyond the scope of this chapter. However, in some cases, pain control may require the use of drugs if therapy for the underlying disease has not eliminated the pain. In this situation, specific treatment recommendations may be given, depending on the clinical characteristics of the pain.

Below are some of the most common types of secondary headaches.

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Post-traumatic headache

Chronic headache may occur after closed or open head injury and after neurosurgery. The severity of headache is often out of proportion to the severity of the injury. Posttraumatic headache most often resembles primary tension-type headache in character. In a series of 48 patients with chronic posttraumatic headache, 75% had headaches classified as tension-type, 21% had headaches that were virtually indistinguishable from migraine without aura, and 4% had “unclassifiable” headaches. Mixed headache patterns are quite common in this situation. Headaches occurring daily are usually described as constant, non-pulsating pain that may be interrupted by severe migraine-like attacks and/or frequent, short-lived episodes of sharp, piercing pain. According to the classification of the International Headache Society, headache that regresses within 8 weeks after injury is designated as acute, while headache that persists beyond this period is designated as chronic.

Headache after craniotomy is highly variable and may include pain and tenderness at the site of the surgical wound; a squeezing or pressing discomfort similar to a tension headache; or a throbbing pain characteristic of migraine. Postoperative pain is not usually accompanied by nausea, vomiting, or photophobia; however, these migraine-like symptoms sometimes occur.

There are several approaches to treating post-traumatic headache. Cognitive and behavioral methods, such as biofeedback or relaxation techniques, are often effective in providing patients with tools to manage chronic pain. There are only a few reports of clinical trials of drugs in post-traumatic headache. One uncontrolled study found that amitriptyline resulted in improvement in 90% of patients. There are isolated reports of positive effects of doxepin, nortriptyline, imipramine, and selective serotonin reuptake inhibitors. Valproic acid or gabapentin, alone or in combination with amitriptyline, may be effective in treating post-traumatic headache. These drugs are particularly useful in the presence of post-traumatic epilepsy. Physical therapy is useful for persistent muscle spasms, and antidepressants are useful for concomitant depression and anxiety.

Infections as a cause of headaches

Headache may occur with various systemic and intracranial infections. It may accompany a common cold or be a threatening sign of a serious CNS infection that can lead to death, which makes it necessary to analyze headache in the context of other symptoms. Below is a brief overview of the most important infectious causes of headache, the treatment of which is carried out using antibacterial agents and/or surgical intervention.

Meningitis is an inflammation of the meninges caused by bacteria, viruses or fungi. Clinical manifestations of meningitis may develop after a short-term systemic disease or manifest without any previous episode. Characteristic symptoms of meningitis are intense headache, fever, neck pain, photophobia, rigidity of individual muscle groups. In addition, epileptic seizures, skin rashes, and depression of consciousness are possible. Urgent examination should include lumbar puncture (in the absence of optic disc edema). In the presence of focal symptoms (e.g., unilateral paresis, oculomotor disorders, pupillary changes, depression of consciousness), CT should be performed immediately, preferably with contrast, to exclude a tumor of the posterior cranial fossa, abscess or hematoma, in which case lumbar puncture may be dangerous. However, if bacterial meningitis is suspected, waiting for neuroimaging should not delay the initiation of antibiotic therapy or serve as a reason to delay lumbar puncture for any length of time.

Meningoencephalitis involves inflammation of both the membranes and the substance of the brain. It may be caused by a viral infection, such as herpes meningoencephalitis. Meningoencephalitis often follows a brief flu-like illness and may clinically resemble meningitis, although its onset is usually less sudden. Seizures or mental status changes may precede other symptoms by several days. CSF examination may reveal elevated protein levels and lymphocytic pleocytosis. CT and MRI findings of temporal lobe involvement also support the diagnosis.

A brain abscess is caused by a bacterial infection and is a focal collection of inflamed, molten necrotic tissue within the brain. It may develop as a result of contact or hematogenous spread of infection and is most often caused by streptococci, staphylococci, and anaerobes. Headache, vomiting, focal neurological symptoms, and decreased consciousness result from compression of surrounding structures and cerebral edema.

Subdural empyema is a collection of pus between the brain parenchyma and the dura mater, manifested by headache, vomiting, decreased consciousness, and focal neurological symptoms.

AIDS can cause headaches during the acute and chronic phases of HIV infection, as well as in connection with accompanying opportunistic infections, such as toxoplasmosis or cryptococcosis. Headaches can also be caused by side effects of drugs used to treat both HIV infection (for example, zidovudine or lamivudine) and opportunistic infections (fluconazole, amphotericin B).

Acute sinusitis may cause pain in the forehead and face. The presence of other signs, such as darkening of the sinuses on radiography or transillumination, fever, purulent nasal discharge, is necessary to confirm the diagnosis and begin antibiotic therapy. Many people mistakenly believe that any pain in the frontal area necessarily indicates sinusitis. Sinusitis of the main or maxillary sinuses can mimic migraine.

Respiratory and systemic viral infections can cause mild to moderate headaches. These "minor" infections do not cause neck stiffness, photophobia, or altered consciousness.

Vascular diseases and headaches

Severe headache may be a manifestation of occlusion of intracranial vessels or leakage of blood through a weakened or damaged vascular wall. Blood spilled into the subarachnoid space is a strong chemical irritant that can cause intense headache and stiffness of the neck muscles. Cerebral ischemia can also cause headache. The following vascular lesions can cause headache.

Subarachnoid hemorrhage most often results from leaking blood from a ruptured cerebral aneurysm and is a neurosurgical emergency. The diagnosis can be confirmed by CT or lumbar puncture. The aneurysm can be identified by angiography.

Below are the symptoms that suggest subarachnoid hemorrhage and require urgent examination with CT and/or lumbar puncture.

1. Sudden onset of pain that reaches maximum intensity within a few seconds.
2. Significant intensity of pain, which the patient often describes as “the worst headache he has ever experienced in his life.”
3. Stiffness of the neck or back muscles due to their contraction.
4. Rapid depression of the level of consciousness due to compression of the trunk.
5. Other less specific signs include photophobia and vomiting.

The development of a full-blown subarachnoid hemorrhage may be preceded by precursor episodes involving small amounts of blood leaking out and having a similar nature but lesser intensity than the main episode. These precursor episodes require careful investigation, since a massive hemorrhage may occur in the near future (usually within 2 to 14 days). Minor focal symptoms may also develop due to compression of adjacent structures by the enlarging aneurysm.

Subdural hematoma is a collection of blood between the dura mater and the surface of the brain, most often manifested by a monotonous, persistent headache. Subdural hematoma can occur even after a mild head injury, but sometimes it develops spontaneously, especially in older people and patients taking anticoagulants.

Cerebellar hemorrhage is a condition that requires urgent neurosurgical intervention and is manifested by headache in the occipital regions, followed by rapid development of signs of brainstem compression, such as decreased consciousness, impaired pupillary innervation, oculomotor disturbances, or paresis.

Arteriovenous malformations (AVMs) are congenital vascular anomalies that bypass capillaries and drain blood from arteries into venous structures. AVMs can cause ipsilateral headache, which in some cases is accompanied by visual and sensory symptoms resembling migraine aura. AVMs are sometimes detected by listening to a murmur over the orbit or head. AVMs can also cause hemorrhages, which lead to more intense headache and focal neurological symptoms.

Occlusion of intracerebral arteries with development of infarction may sometimes be accompanied by headache. However, in general, focal neurological symptoms, rather than headache, dominate the clinical picture of ischemic stroke. Occlusion of the cerebral venous sinus may also be associated with headache and focal neurological defect. Cavernous sinus thrombosis manifests itself as intense eye pain and scleral injection, which are accompanied by damage to the III, V ₁ V ₂ and VI cranial nerves. Sagittal sinus thrombosis may manifest itself as headache, epileptic seizures and focal neurological symptoms.

Carotid artery dissection occurs when blood separates the muscular layers of the vessel wall following damage to the intima. Carotid artery dissection may occur after seemingly minor head or neck trauma (such as a taxi driver turning their head abruptly) and presents with intense head and neck pain that may radiate to the eyebrow, eye, orbit, or mastoid region. The following neurological symptoms may occur with carotid artery dissection:

1. paralysis of the tongue due to damage to the 12th nerve (probably due to mechanical compression of the ansa cervicalis in the neck);
2. Horner's syndrome with involvement of the sympathetic fibers of the perivascular plexus.

Treatment may involve anticoagulants for 3 months, followed by antiplatelet agents for a similar period. Resection of the residual dissecting aneurysm, a possible source of embolism, may be required if such an operation is technically feasible.

Intracranial tumors as a cause of headaches

Many patients believe that their headaches are a manifestation of an undiagnosed brain tumor. Fortunately, in the vast majority of cases, headaches are not associated with any structural changes. However, it is important to be able to diagnose intracranial tumors.

Of 111 patients with a brain tumor confirmed by CT or MRI, Forsyth and Posner (1992) noted chronic headache in 48% of cases. Pain caused by the tumor is usually monotonous and bifrontal, but is often worse on the ipsilateral side. In its characteristics, this pain is more often close to tension headache (77%) than to migraine (9%), and is often intermittent and moderately intense (the average score on a 10-point scale is 7 points). The pain is accompanied by nausea for about half of its duration. Headache arising against a background of increased intracranial pressure is usually resistant to traditional analgesics. "Classic" headache in brain tumors, occurring in the morning, was noted in only 17% of patients.

Brain tumors do not have a specific headache pattern. Signs that suggest an intracranial tumor include swelling of the optic discs, new neurological symptoms, a prolonged headache episode that first occurs after age 45, a history of cancer, increasing cognitive impairment, or decreased consciousness.

The pain may regress after resection or radiotherapy of the tumor. If surgery is planned in the near future, aspirin and other nonsteroidal anti-inflammatory drugs should be avoided because they increase the risk of bleeding. If surgery is not possible, symptomatic therapy is necessary. Mild to moderate headache is effectively treated with conventional analgesics, while severe headache may require narcotic analgesics. Perifocal edema can be reduced with a corticosteroid (dexamethasone, 4 mg orally every 6 hours) or mannitol (200 mL of a 20% solution intravenously every 8 hours), either of which may relieve headache secondarily.

Autoimmune and inflammatory diseases as causes of headaches

Temporal (giant cell) arteritis is a disease characterized by inflammatory lesions of the branches of the carotid arteries, primarily the temporal artery. It usually affects people over 60 years of age and can lead to rapid and irreversible loss of vision due to granulomatous lesions with occlusion of the posterior ciliary artery or central retinal artery. The following indicate temporal arteritis:

1. pain in the orbital or frontal-temporal region, which has a monotonous, constant character, sometimes with a pulsating sensation;
2. increased pain when exposed to cold;
3. pain in the lower jaw or tongue, which intensifies when chewing (“intermittent claudication” of the lower jaw);
4. additional general symptoms: weight loss, anemia, mononeuropathy, changes in liver function tests;
5. decreased visual acuity, visual field defects with pallor or edema of the optic discs and dissecting hemorrhages in the retina (in anterior ischemic optic neuropathy) or pallor of the retina with the presence of a cherry-red spot (in occlusion of the central retinal artery).

Timely adequate therapy is important, since transient visual impairment can quickly turn into irreversible blindness. If temporal arteritis is suspected, it is necessary to immediately begin treatment with corticosteroids to avoid vision loss, which in 75% of cases becomes bilateral after unilateral. In 95%, an increase in ESR is noted. The diagnosis can be confirmed by biopsy of the temporal artery, which makes sense to perform no later than 48 hours after the start of corticosteroid therapy.

If ESR increases, methylprednisolone is prescribed, 500-1000 mg intravenously every 12 hours for 48 hours, after which they switch to prednisolone orally at a dose of 80-100 mg per day for 14-21 days, followed by gradual withdrawal of the corticosteroid over 12-24 months. The rate of withdrawal is determined by the dynamics of ESR.

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Tolosa-Hunt syndrome

Granulomatous process in the cavernous sinus or superior orbital fissure, manifested by painful ophthalmoplegia and decreased sensitivity in the forehead. Treatment consists of corticosteroid therapy.

Headache may be a manifestation of collagenoses, autoimmune angiopathies, such as isolated CNS angiitis. Headache usually decreases after treatment of the vasculitis that is its cause.

Toxic-metabolic disorders

Exogenous substance-induced headache may occur as a result of direct exposure to certain substances or as a result of withdrawal symptoms in individuals who regularly take psychoactive substances.

Metabolic disorders

Headache can be a manifestation of various metabolic disorders. The following types of headache can be attributed to this group.

1. Headache with hypercapnia occurs with an increase in pCO2 _> 50 mm Hg in the absence of hypoxia.
2. Hypoglycemic headache occurs when blood sugar levels fall below 2.2 mmol/L (< 60 mg/dL).
3. Dialysis headache occurs during or shortly after a hemodialysis session (to eliminate the headache, the dialysis rate should be reduced).
4. High-altitude headache usually occurs within 24 hours of rapid ascent to altitudes above 10,000 feet (3,000 m). The headache is accompanied by at least one other symptom of altitude sickness, including Cheyne-Stokes respiration at night, severe shortness of breath with exertion, or a desire to take deeper breaths.
5. Headache caused by hypoxia is usually observed in low ambient pressure or pulmonary disease when arterial _P02 falls below 70 mm Hg.
6. Headache in sleep apnea is likely related to hypoxia and hypercapnia.

Substances that cause headaches

Substances that directly cause headaches

• Alcohol
• Amphotericin B
• Verapamil
• Danazol
• Diclofenac
• Dipyridamole
• Ivdometacin
• Cocaine (crack)
• Sodium monoglutamate
• Nitrates/nitrites
• Nifedipine
• Ondansetron
• Ranitidine
• Reserpine
• Tyaramin
• Carbon monoxide
• Phenylethylamine
• Fluconazole
• Cimetidine
• Estrogens/oral contraceptives

Substances that cause withdrawal headaches

• Alcohol
• Barbiturates
• Caffeine
• Opioid analgesics
• Ergotamine

Eye diseases and headaches

Headache may occur in patients with eye diseases, in particular, with two forms of glaucoma.

1. Pigmentary glaucoma is a form of open-angle glaucoma that occurs when pigment from the iris is released into the fluid in the anterior chamber of the eye during physical exertion. As a result, the outflow of fluid through the trabecular system is blocked. This condition most often occurs in young men with myopia and is characterized by headaches and blurred vision, which are provoked by physical exertion.
2. Acute angle-closure glaucoma - characterized by blockage of free flow of fluid through the pupil, which leads to anterior displacement of the iris and obstruction of the trabecular system. It manifests itself as dilated pupils with no reaction to light, blurred vision, intense pain in the eyeball, clouding of the cornea and a marked increase in intraocular pressure. Episodes are provoked by dilation of the pupils under the influence of physiological or pharmacological factors.

Both types of glaucoma require immediate referral to an ophthalmologist. In acute angle-closure glaucoma, laser iridotomy is often indicated. Glaucoma is sometimes confused with cluster headaches. However, in cluster headaches, the pupil constricts rather than dilates, and ptosis is often present.

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Arterial hypertension as a cause of headache

A sharp increase in blood pressure (when diastolic pressure exceeds 120 mm Hg) can be the cause of headache. Pain in arterial hypertension is often diffuse and is usually most pronounced in the morning, gradually weakening over the next few hours.

Four types of headaches are associated with severe arterial hypertension.

1. Acute hypertensive reaction to an exogenous substance. Headache occurs in temporary connection with the rise in blood pressure under the influence of a specific toxin or drug and disappears within 24 hours after the blood pressure is normalized.
2. Preeclampsia and eclampsia. During pregnancy, labor, and the early postpartum period, headache may be accompanied by other manifestations of preeclampsia, including increased blood pressure, proteinuria, and edema. Headache usually regresses within 7 days after a decrease in blood pressure or resolution of pregnancy.
3. Pheochromocytoma, a tumor of the adrenal gland that secretes norepinephrine or adrenaline, can cause short-term headaches accompanied by sweating, anxiety, palpitations, and a sharp rise in blood pressure.
4. Malignant hypertension with acute hypertensive encephalopathy causes headache, grade 3 or 4 retinopathy, and/or decreased consciousness. In this case, there is a temporary relationship between the headache and the episode of high blood pressure; after the blood pressure decreases, the pain disappears within 2 days.

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Decrease and increase in intracranial pressure

Headache with intracranial hypotension is possible with a decrease in intracranial pressure (ICP) to 50-90 mm H2O, which is usually caused by a decrease in the volume of cerebrospinal fluid and often causes a monotonous pulsating headache, sometimes quite intense. It is probably explained by a decrease in the "cerebrospinal fluid cushion" and elasticity of the brain, which leads to tension of the meningeal and vascular structures that have pain receptors. Pain with intracranial hypotension increases in an upright position and decreases in a horizontal position. Headache can begin gradually or suddenly and is accompanied by dizziness, visual impairment, photophobia, nausea, vomiting, and sweating. Although headache with intracranial hypotension can begin spontaneously, it most often develops after a lumbar puncture (LP). Other causes of intracranial hypotension include intracranial surgery, ventricular shunting, trauma, various systemic disorders such as severe dehydration, post-dialysis state, diabetic coma, uremia, hyperventilation. In persistent headache, a CSF fistula should be excluded by radionuclide cisternography or CT myelography.

Postdural puncture headache is caused by excess leakage of cerebrospinal fluid through the hole in the dura mater made by the puncture needle. Headache occurs in 10% to 30% of cases after lumbar puncture, twice as often in women as in men. Headache may begin within minutes to several days after the puncture and persist for two days to two weeks. Treatment may include corticosteroids, oral fluid and salt intake, intravenous fluids, CO ₂ inhalation, and methylxanthines such as theophylline 300 mg three times daily, caffeine 500 mg intravenously, or endolumbar autologous blood to seal the defect in the dura mater.

Headache with increased intracranial pressure (intracranial hypertension) is caused by deformation of dural and vascular structures that are sensitive to pain, or direct pressure on cranial nerves that conduct pain impulses, such as the trigeminal nerve. Although the localization of this type of headache is variable, most often the pain is bilateral and localized in the frontal-temporal region. Increased ICP can be caused by space-occupying lesions, blockage of cerebrospinal fluid circulation, hemorrhages, acute hypertensive encephalopathy, venous sinus thrombosis, adrenal hyper- or hypofunction, altitude sickness, tetracycline or vitamin A intoxication, and many other conditions. In most cases, the cause of increased intracranial pressure and headache can be determined. Treatment of the underlying disease usually leads to regression of the headache.

Idiopathic intracranial hypertension (pseudotumor cerebri) is a condition characterized by headache, papilledema, and transient episodes of blurred vision that occur in the absence of any changes in the cerebrospinal fluid other than increased intracranial pressure. However, in one clinical series of 12 patients, papilledema was not detected. The condition is not associated with hydrocephalus or other identifiable causes. Idiopathic intracranial hypertension occurs 8-10 times more often in women than in men. The typical patient is an overweight woman of childbearing age.

The diagnosis of idiopathic intracranial hypertension is confirmed by lumbar puncture (CSF pressure >250 mmHg with normal CSF composition) and neuroimaging that excludes a space-occupying lesion or hydrocephalus. Visual field examination often reveals enlargement of the blind spot. Although spontaneous recovery is common, measures to reduce intracranial pressure are usually necessary because of the risk of visual loss. Frequently repeated LP are sometimes effective but are associated with a risk of complications, including postdural puncture headache, brain herniation, spinal epidermoid tumor, or infection. Pharmacotherapy is aimed primarily at reducing CSF production and includes acetazolamide and furosemide. Furosemide, a potent loop diuretic, should be given with potassium supplements, and its potential to cause hypotension should be taken into account. Surgical treatment consists of fenestration of the optic nerve canals and ventriculoperitoneal shunting.

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