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Vascular Headaches

Cranial Arteritis

Cranial arteritis, a form of giant cell arteritis, involves the branches of arteries arising from the thoracic aorta, such as the temporal and ophthalmic arteries, and the ophthalmic and intracranial vessels. The condition only affects people over the age of 60 years. If untreated, it leads to blindness in half of the cases. The leading symptom—a mild to moderate, constant, unilateral temporal pain—moves between head regions and is associated with local tenderness and redness over the scalp. The temporal arteries are typically tender, cordlike, and often pulseless. Accompanying the headache may be painful "angina" of the jaw muscles or tongue when chewing or swallowing or dental pain that may lead to misguided extractions. Confusion, impaired concentration, aphasia, and other focal signs reflect intracranial artery involvement. Repeated episodes of blurry or blotted-out areas of vision may precede complete loss of vision in one or both eyes. The patient often feels unwell, with low-grade fever, anorexia, malaise, and symptoms such as morning muscle stiffness and weight loss. An elevated erythrocyte sedimentation rate (ESR) and positive antinuclear antibody (ANA) titers are almost always present. The differential diagnosis includes depression, hypertension, cervical degenerative joint disease, and recurrent migraine.

Temporal artery biopsy is not essential but can be obtained from the most tender and inflamed area of an artery to confirm the diagnosis, even after treatment has been started. Delay in therapy may allow serious vascular events (e.g., retinal artery occlusion) to occur. The value of having a biopsy may be appreciated after several months, when the potential complications of steroid therapy threaten and questions arise as to the veracity of the diagnosis. Doppler flow studies may also help identify areas in the superficial cranial circulation where occlusion is taking place and the process is active.

Immediate treatment with steroids is essential; prednisolone (100 mg/day initially, reduced gradually to a maintenance dose of 5 mg/day) with medication to prevent gastric ulceration (such as ranitidine, 150 mg bid) is appropriate. Gradual tapering of this dose is indicated over weeks and months (and occasionally years) in relation to symptoms and the decreasing ESR. If steroid therapy is contraindicated (active infection, active gastrointestinal ulceration or perforation, serious CNS reaction to steroids), other NSAIDs may be tolerated and prove useful. In some patients the arteritis may continue to be active over 3 to 4 years, with symptoms recurring whenever the steroid dose falls below a certain level. In patients with long-term arteritis, alternate-day steroid therapy to reduce side effects may be practical.

Hypertension

In hypertensive encephalopathy and crises related to pheochromocytoma and preeclampsia, a sudden rise in blood pressure leads to headache. Hypertension associated with Cushing's syndrome or with aldosterone-producing tumors may also cause headache of a vascular type resembling migraine in a few patients.

Dialysis Headache

Almost all patients on dialysis experience headache if the dialysate contains too little sodium. Dialysis headache is related to reduction in osmolality caused by large sodium decreases and worsens as blood pressure drops . Headache also is one of the first symptoms of transplant rejection.

Headache from Dissection of the Carotid Artery

Acute carotid dissection may cause sudden, severe, unilateral neck pain and headache radiating to the ear, temple, and eye. An ipsilateral Horner's syndrome is the only physical sign unless there is evidence of a TIA or stroke from embolism. During the acute phase the carotid sheath is tender, the pulse is poorly felt, and a carotid bruit may be heard. The patient should be referred for MRA or angiography. There is no evidence to support the use of anticoagulants, but they are commonly prescribed.

Migraine and Mitral Valve Prolapse (Barlow's Syndrome)

Patients with migraine have an increased incidence of mitral valve prolapse (MVP), which may be responsible for the increased frequency of paroxysmal cardiac arrhythmias reported in patients with migraines. Small cerebral emboli in patients with MVP may simulate classic migraine attacks. Some patients have positive anticardiolipin antibody tests and need specialized assessment. Propranolol is used to treat MVP and so may serve a double purpose. Antiplatelet agents are also used in prophylaxis.

Headache after Ischemic Cerebral Infarction

After a stroke, many patients complain of a headache that has a vague resemblance to migraine without aura, as first described by Thomas Willis in the seventeenth century. A possible reason is the increase in blood flow in the scalp vessels when a major artery such as a carotid has been occluded. Analgesics are appropriate as therapy in the short term. In many cases the headache fades spontaneously over months. Use of vasoconstrictors is obviously inappropriate.

Headache Caused by Intracranial Bleeding

The profile of an attack of headache resulting from intracranial hemorrhage from aneurysms or arteriovenous malformations (AVM) is shown in Fig. 160-6. Such lesions rarely cause headache except when they bleed, although in exceptional cases headache may result from pressure of an aneurysm on pain-sensitive structures. The usual presentation is acute: the patient experiences sudden posterior head pain that feels like a hammer blow without apparent cause, although it may occasionally be related to physical stress such as sexual intercourse or weight lifting. In other cases the headache is only minor and may recur repeatedly before a major, perhaps fatal event. If the bleeding is into the subarachnoid space, stiff neck, fever, backache, and severe, sudden headache result. If it extends intracerebrally, local neurologic deficits result. In severe cases, such as subarachnoid hemorrhage caused by rupture of an aneurysm, spread of blood into the ventricles is often fatal. Smaller leaks from an AVM tend to recur and are far less dangerous. Differentiation of either of these from benign exertional headaches is clinically impossible and, at least on the first occurrence, full investigation is essential.

Any acute, severe headache, even without stiff neck or other physical signs, should be regarded as evidence of subarachnoid hemorrhage until proved otherwise by CT scan and perhaps LP. Immediate consultation with a neurologist or neurosurgeon is indicated in all such cases. A small subarachnoid leak (producing a "sentinel headache") will lead to such a severe headache without physical signs. Initially, this should be managed exactly as would a full-blown subarachnoid hemorrhage.

A condition similar to headache caused by intracranial bleeding is exertional headache (including "coital cephalgia" and "weight-lifters headache"), which is manifest by the occurrence of a severe, acute, usually posterior head pain at times of maximal muscular activity—as suggested by the alternate names for the condition. The first time this happens should be the occasion for full investigation (CT scan of the head, and perhaps LP) to exclude a small subarachnoid bleed. If these rule out subarachnoid hemorrhage, and the activity is to be repeated, indomethacin, 25 mg tid, is an effective prophylactic.

The nature of cough headache is unexplained. Its characteristics are those of exertional headache and it occurs at times of violent coughing or during the performance of Valsalva's maneuver. In such cases, the presence of an intracranial mass lesion is possible and must be excluded by appropriate examination and scanning. The Chiari malformation is another, more benign cause.