Negative impact of depression on outcomes in patients with coronary artery disease: mechanisms, treatment considerations, and future directions.

Depressive symptoms are common in coronary artery disease (CAD) patients, and are associated with increased cardiac risk. Although an important relation exists between depression and CAD prognosis, the underlying pathophysiological mechanisms are poorly understood. Additionally, evidence including the recently published ENRICHD (Enhancing Recovery in Coronary Heart Disease Patients) trial suggests that depression treatments do not lower recurrent cardiac risk. The reason for the observed lack of benefit with depression treatment in CAD patients is unclear. In this review, we discuss the impact of depression in CAD patients, the possible mechanisms involved, the studies that have examined the effects of psychological and antidepressant therapies on recurrent cardiac events, and the direction that future research should take.

"Abdominal crunch"-induced rhabdomyolysis presenting as right upper quadrant pain.

A young, active duty sailor presented with right upper quadrant abdominal pain. History, physical, and laboratory findings initially suggested cholecystitis or related disease. Further evaluation found myoglobinuria and a recently increased exercise program, leading to the diagnosis of exercise-induced right upper abdominal wall rhabdomyolysis. Although not a common cause of abdominal pain, this diagnosis should be considered in the patient with abdominal pain and a recently increased exercise program, particularly exercises of the abdominal wall such as "abdominal crunches."

Chronic post-traumatic headaches classified and compared with natural headaches.

This study sought to determine whether chronic post-traumatic headaches are different from or identical to the naturally occurring headaches. The chronic post-traumatic headaches of 48 patients were classified, as if they were natural headaches, by the diagnostic criteria of the International Headache Society. Thirty-six patients' headaches (75%) were chronic tension-type headache, 10 (21%) were migraine without aura, and 2 (4%) were unclassifiable. The characteristics and accompaniments of the headaches within each diagnostic group were then compared to those in a control group with natural headaches of the same type. No notable differences between the post-traumatic and control groups were found. Hence, chronic post-traumatic headaches have no special features, but are symptomatically identical to either chronic tension-type headache or migraine without aura (in this series of patients). This identity suggests that post-traumatic headaches are generated by the same processes causing the natural headaches, not by intracranial derangement from head blows or jolts.

Continuous chronic tension-type headache unaffected by two hours of frontalis and trapezius relaxation.

Fourteen patients with the continuous form of chronic tension-type headache maintained electromyographically documented relaxation of frontalis and trapezius muscles for two consecutive hours. The headache intensity of the group did not decrease from the beginning to the end of the recording session. This result is evidence against tonic muscle tension as the mechanism of this form of headache.

Headache caused by a single lesion of multiple sclerosis in the periaqueductal gray area.

We report a severe acute headache that occurred in conjunction with a solitary fresh lesion of multiple sclerosis in the periaqueductal gray region of a 16-year-old girl. This unique natural event supports the recent proposition, based on observations of patients with implanted electrodes, that perturbations of the periaqueductal gray region can produce headache. It also suggests that headaches accompanying attacks of multiple sclerosis are due to disturbances in particular regions of the brain.

Arteriovenous malformations and migraine: case reports and an analysis of the relationship.

Some patients with cerebral arteriovenous malformations (AVMs) suffer recurrent migrainous attacks which meet the official criteria for migraine. The relationship of these attacks to the malformations has been poorly substantiated. Instances where attacks disappeared following surgical extirpation of an AVM support a relationship, but several other reported surgical outcomes do not. Both patients presented here had surgical results seemingly antithetical to a relationship: the attacks persisted in the first patient and began in the second after removal of the AVM. Nevertheless, data assembled from the literature attests to a causal role for AVMs in the production of migrainous attacks, by showing an overwhelming correlation between the side of the cranium with the AVM and the side afflicted by unilateral headache. An equally good correlation exists for lateralized auras. The correlative and surgical data together show that migrainous attacks develop in relation to AVMs, but not within the malformation itself. Instead, the neighboring brain is probably the generative site.

Plasmapheresis alleviates neuropathy accompanying IgM anti-myelin-associated glycoprotein paraproteinemia.

A patient with peripheral neuropathy accompanying a benign IgM anti-myelin-associated glycoprotein paraproteinemia has been treated successfully by plasmapheresis for over a year, and during this time, fluctuations in the patient's symptoms and signs have correlated with variations in the serum IgM level. These results suggest that plasmapheresis may be more beneficial for such neuropathies than indicated previously, and they add to the evidence implicating the paraprotein as the cause of the neuropathy.

Trauma-triggered migraine: an explanation for common neurological attacks after mild head injury. Review of the literature.

This paper reviews the literature on complex temporary disturbances of brain function triggered by mild blows to the head in children, adolescents, and young adults. It consolidates the evidence by which these attacks have been identified as classical or complicated migraines, and provides a historical account of the descriptions and proffered explanations of these attacks. The clinical features and the electroencephalography, angiography, computerized tomography, and cerebrospinal fluid findings of trauma-induced migraine are presented and compared to those of spontaneous migraine. Ideas about the pathogenesis of this condition are related to current thinking on the neurological phenomena of migraine in general.

Transient global amnesia triggered by mild head trauma.

In 9 patients, aged 11 to 28 years, minor head injury triggered an amnesic attack grossly disproportionate to the degree of trauma. During these attacks, patients were unable to form new memories for 2 to 24 hours, had extensive retrograde amnesia, voiced repetitive queries and were disorientated for time, but were otherwise intact neurologically. We suggest that these episodes were attacks of transient global amnesia triggered by the mild blows to the head. We also suggest that they constitute a previously unrecognized variety of traumatic migraine.

Role of angiotensin in lethal cerebral hypoperfusion during treatment of acute hypertension.

A 23-year-old man developed lethal cerebral hypoperfusion associated with angiographically demonstrable cerebral arterial spasm while being treated for acute angiotensinogenic hypertension due to a traumatic coarctation of the aorta. This complication occurred even though the treatment maintained his blood pressure at normotensive to mildly hypertensive levels, without producing more than rare and fleeting periods of hypotension. To explain this enigmatic development, we propose that the high concentration of angiotensin II in the blood constricted the cerebral arteries and thus prevented adequate cerebral autoregulation when his blood pressure was lowered by drug therapy.

Death from cerebral hypoperfusion during nitroprusside treatment of acute angiotensin-dependent hypertension.

A 37-year-old woman, while being treated with nitroprusside for acute hypertension due to an intramural renal artery hemorrhage, became blind on the fourth hospital day, comatose on the fifth, and brain dead on the seventh. Postmortem examination of her brain revealed border-zone infarcts in the parietal-occipital regions and cerebrellum of the sort associated with cerebral hypoperfusion due to hypotension. Yet her blood pressure had been lowered judiciously to a mean pressure in the vicinity of 110 to 120 mm Hg, and episodes of hypotension had been avoided. As possible explanations for this unusual complication, the roles of acute hyperangiotensinemia and nitroprusside administration are discussed.