4.4: Benign cough headache

Cough headache was the subject of an interesting paper written by Sir Charles Symonds (1956). He remarked that coughing may aggravate headache as observed in some patients with intracranial tumors, but his paper primarily concerns those patients in whom immediate and transient pain is initiated by coughing. Symonds divided the cases he had studied into groups. In one group, he placed six patients in whom cough headache was associated with an organic lesion. The organic involvements in these cases were: meningioma below the tentorium and extending to the torcula; a midbrain cyst; three cases of Paget's disease with basilar impression; and a patient in whom the cough headache commenced a few weeks after the removal of an acoustic neuroma. In these and other cases, coughing, sneezing, laughing, or straining at stool was sufficient to initiate pain in the head, usually of brief duration (a few minutes or less) and variously situated from the posterior occipital to the frontal and temporal regions and sometimes affecting the neck. Symonds cited several observers who had noted that pain may result from traction on dural sinuses and that stimulation of the transverse sinus and torcula may result in headache involving the forehead and eye. He remarked that adhesions between the arachnoid and dura are particularly likely to produce pain and concluded that increased pressure within the posterior fossa is important regarding cough headache.

Rooke (1968) found that 10% of 103 patients he examined with cough or other exertional headache had intracranial lesions, primarily in the posterior fossa. The commonest abnormality that Rooke encountered was the Chiari malformation with basilar impression, although other causes of exertional headache included subdural hematoma as well as brainstem, cerebellar, and hemispheric tumors.

Symonds (1956) encountered 21 patients who had cough headache but in whom there was no evidence of organic disease. He placed these patients in two groups: those who experienced headache only on provocations such as have been mentioned (14 cases), and the remainder (7 cases) in whom cough headache was present but spontaneous headaches had preceded the type of headache under consideration. Of the 21 patients, 15 enjoyed recovery from cough headache after periods of up to 12 years. In this group of cases, Symonds (1956) suspected some type of posterior fossa involvement of transitory nature largely because some of the patients had disturbed auditory or vestibular function.
In Rooke's (1968) study, most of the patients were males, with a mean age of 55 years. In those 93 patients who had no evidence of intracranial disease, 30 were free of headache within 5 years, and 73 were improved or free of headache after 10 years. Rooke also found that the headaches in some patients resolved after dental extractions or lumbar puncture, while other patients responded dramatically to treatment with indomethacin.

Diamond (1982) evaluated 15 patients with what he has termed ``prolonged benign exertional headache.'' In all patients, the headaches occurred during one or several of the following maneuvers: (1) those that raise intrathoracic pressure, such as coughing, sneezing, defecating, laughing, crying, stooping, lifting, etc., and (2) circumstances that may suddenly raise the blood pressure, such as excessive exercise or orgasm. Diamond also found that these headaches responded to indomethacin. The mechanism of exertional headaches in patients with and without intracranial lesions is unclear.
From the studies of Symonds (1956) and of Rooke (1968), it would seem that headache initiated by cough may indicate organic disease that includes posterior fossa (and particularly foramen magnum) pathology in 10---20% of cases, but that in a large majority of cases, the symptom complex cannot be explained with certainty although ultimate recovery is probable, with or without the use of indomethacin. Because 1/10 to 1/5 have definite pathology, all patients with this condition must have magnetic resonance scans. Nightingale and Williams (1987) believe that the Arnold-Chiari malformation is underrecognized as a cause of the syndrome.

Raskin (1988) has characterized the temporal profile of some patients with cough headache. Many of his patients note their headache during lower respiratory infections accompanied by severe coughing or during strenuous weight-lifting. The headache arises moments after sufficient stimulus, reaches its peak almost immediately, and then subsides over several seconds to a few minutes, usually conforming to a "spike" when graphically illustrated by patients. Occasional patients report their pain remains at a peak for several seconds before it tails off (Figure 36.1). This temporal profile differentiates it from benign exertion headache (see below). As pointed out by Raskin (1988), it should be appreciated that many headache syndromes are worsened by coughing or bending, but in this syndrome of cough headache a paroxysm is elicited. In effort migraine, headache usually appears during protracted exertion such as during the fourth or fifth mile of the prolonged distance runner or after the exercise has been completed. The duration of effort migraine is usually many hours rather than seconds to minutes.

Raskin (1988) reviewed the pathophysiology. It seems that the headache occurs or is elicited by a sudden increase in intracranial pressure (ICP). Therefore, it is a reverse relationship to lumbar puncture headache which is induced by sudden lowering of ICP and spinal fluid volume which can be stopped by an increase in intracranial pressure in ICP. Coughing, lifting, and straining result in increased intra-thoracic and intraabdomenal pressure impeding the venous return to the right side of the heart, thus increasing central venous pressure and, therefore intracranial pressure. Increase in venous pressure is transmitted to the jugular venous system into the epidural venous plexus. Blood coming into the epidural venous plexus compresses the dura, further contributing to heightened pressure within the CSF. It has been documented (Williams 1976) that after cough there is an increase in lumbar CSF pressure as well as cisternal pressure. Increased pressure on the pain sensitive dura may be responsible for the headache, but the exact receptors have not been identified. With an Arnold-Chiari malformation and cerebellar tonsillar herniation there may be a valve-like blockade at the foramen magnum producing a craniospinal pressure dissociation (Raskin 1988). Cough headache is a characteristic of this syndrome and it disappears after decompression of the cerebellar tonsils. However, it should be stressed that most patients with the cough headache syndrome do not have Arnold-Chiari malformation. The long-term outlook for patients is favorable and many of the patients respond to indomethacin. Raskin reports that should indomethacin fail that naproxen, ergonovine, and phenelzine would be useful as backup. Interestingly enough, beta-blockers seem to be particularly ineffective in this syndrome.

 

 

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