When and how to investigate the patient with headache.

The common complaint of headache usually has a benign cause, most often a primary headache syndrome. The history and neurologic and general physical examinations usually permit a definitive diagnosis. When in doubt, diagnostic testing is indicated. Certain historical and examination findings increase the likelihood of a secondary headache disorder and the need for diagnostic testing. These include (1) recent head or neck injury; (2) a new, worse, worsening, or abrupt onset headache; (3) headache brought on by Valsalva maneuver or cough; (4) headache brought on by exertion; (5) headache associated with sexual activity; (6) pregnancy; (7) headache in the patient over the age of ~50; (8) neurologic findings and/or symptoms; (9) systemic signs and/or symptoms; (10) secondary risk factors, such as cancer or human immunodeficiency virus (HIV) infection. Less worrisome are headaches that wake the patient from sleep at night, always occur on the same side, or show a prominent effect of change in posture on the patient's pain. Diagnostic studies include neuroimaging, cerebrospinal fluid (CSF) examination, and blood tests, which are selected depending on the patient's history and findings. For most patients, the diagnostic test of choice is a magnetic resonance imaging (MRI) brain scan. Computed tomography (CT) of the brain is usually obtained in the setting of trauma or the abrupt onset of headache. CSF examination is useful in diagnosing subarachnoid bleeding, infection, and high and low CSF pressure syndromes.

GABA-ergic system in brain regions of glutamate-lesioned rats.

Subcutaneous administration of high doses of glutamate to rats during their first 10 days after birth produced a great reduction of GABA content and GAD activity in the adult mediobasal hypothalamus, both in male and female. In addition GABA content and GAD activity showed a slight significant decrease in female cerebellum and male striatum. Glutamate treatment was also followed by a significant increase in GABA content and GAD activity of male substantia nigra, cerebellum, hippocampus and of female olfactory bulb. No reduction in GABA-T activity was observed in different brain areas studied except in mediobasal hypothalamus. The results support the view that glutamate treatment had a direct toxic effect on GABA-ergic neurons in mediobasal hypothalamus. The changes in GAD activity observed in all areas studied may reflect the neuroendocrine changes determined by nucleus arcuate lesions.

Effects of thyroxine on methionine adenosyltransferase activity in rat cerebral cortex and cerebellum during postnatal development.

Methionine adenosyltransferase (MAT) activity was evaluated in cerebral cortex and cerebellum in controls and in rats treated with thyroxine. In controls the enzyme showed a different pattern in cerebral cortex and cerebellum during neonatal and late suckling periods. Hyperthyroid rats showed a significant increase of the enzyme in cerebral cortex only at the 2nd day of the neonatal period; in cerebellum the developmental pattern of MAT in neonatal period was anticipated temporally by 2-4 days. During the late suckling period thyroxine treatment produced in cerebellum a significant decrease in MAT activity at the 15th day after birth. From these data, we propose that hyperthyroidism may cause precocious induction of MAT both in cerebral cortex and in cerebellum and that the increased availability of S-adenosyl-L-methionine during the neonatal period could be related to its utilization also in polyamine biosynthesis.