Does patent foramen ovale promote cryptogenic stroke and migraine headache?

Cryptogenic stroke is a diagnosis of exclusion. These are strokes that occur in people who are usually less than 55 years old, without an identifiable cause. Our sensitivity to these events has been heightened because of the new definitions of a transient ischemic attack. Transient ischemic attack (TIA) is a clinical diagnosis of a neurologic deficit without MRI abnormalities: if there is an MRI abnormality, whether or not that person is symptomatic, it is now defined as a stroke. With these new definitions, and the sensitivity of MRI, we are seeing more cryptogenic strokes. It has been hypothesized that many cryptogenic strokes are caused by small emboli that travel from the legs to the right atrium; during straining (such as a Valsalva maneuver) these emboli can go across a PFO into the left atrium and then travel to the brain, producing a stroke. The problem is that these are very small emboli, approximately 1 to 3 mm, and we can't actually show these small emboli crossing from right to left. However, large emboli have been observed by echocardiography to be trapped in the PFO. So the diagnosis of cryptogenic stroke is a diagnosis of exclusion that is impossible to verify. What is the scope of the problem? Of the 700,000 strokes per year in the United States, 80% of them are ischemic, and 20% of those are defined as cryptogenic. The prevalence of PFO among this cryptogenic stroke population is about 40% to 50%; in the general population, it's only about 20%. Current estimates are that somewhere between 30,000 and 60,000 strokes per year in the U.S. are caused by paradoxical embolism through a PFO. There are some other fascinating associations: scuba divers with PFOs are more susceptible to decompression illness. Platypnea-orthodeoxia is a condition of desaturation that occurs when you're standing up but not when you're lying down; these patients are quite symptomatic, with arterial saturations in the low 80s. They also frequently have PFOs; if you close the PFO, the arterial desaturation is alleviated. Fat emboli during orthopedic surgery or air emboli during neurosurgery may also travel through the venous system. If you don't have a PFO, the fat or the air is trapped in the lungs and doesn't cause much of a problem unless it's massive; but if you have a PFO, then the embolus can go from right to left atrium up to the brain, with devastating neurologic consequences.

[Prevalence of systemic and ocular diseases in age-related cataract patients]. / Systemische und okuläre Begleiterkrankungen bei Katarakt-Patienten.

BACKGROUND: Cataract patients often display concomitant ocular and systemic diseases which may influence the decision between general and regional anesthesia. The aim of this study was to quantify co-morbidity of these patients and assess the influence of the two types of anesthesia an the anesthesiological risk on the frequency of intra- and post-operative complications and visual outcome. METHODS: In this prospective study, in patients scheduled for cataract extraction at the University Eye Hospital and Clinic of Ulm (tertiary eye care center) all systemic and ocular diseases as well as intra- and postoperative complications were analyzed. The prevalence of the co-morbidity in our patients was compared to other studies including age-matched controls. The anesthesiological risk was quantified using the classification scheme of the American Society of Anesthesiologists (ASA). RESULTS: Eighty-eight patients with a mean age of 70.4 +/- 11.7 years were analyzed. Sixty-one% of patients displayed systemic as well as ocular co-morbidity. Only systemic or ocular comorbidity was present in 32% and 5% of patients, respectively. Two% of patients exhibited neither ocular nor systemic comorbidity. In 61% of patients the surgery was performed in regional anesthesia and in 39% in general anesthesia. The prevalence of systemic and ocular co-morbidity as found in our study was significantly higher as compared to that in the general population of the same age. Visual improvement and the frequency of intra- and postoperative complications were independent on type of anesthesia and anesthesiological risk. CONCLUSIONS: Patients who were scheduled at our institution for cataract surgery exhibited a high frequency of ocular as well as systemic co-morbidity. This can be interpreted in such a way that patients with a high level of co-morbidity are referred to tertiary eye care centers for cataract surgery.

Improvement of impaired counterregulatory hormone response and symptom perception by short-term avoidance of hypoglycemia in IDDM.

OBJECTIVE: To test the hypothesis that impaired counterregulatory hormone response and symptom perception, induced by recurrent hypoglycemic episodes over 2 days, may be improved by short-term (2-day) avoidance of hypoglycemia. RESEARCH AND DESIGN: We examined two groups of insulin-dependent diabetes mellitus (IDDM) patients (n = 16), none of whom exhibited signs of peripheral or autonomic neuropathy. Two sequential euglycemic-hypoglycemic clamp studies were performed applying stable glycemic plateaus of 5.6, 3.3, 2.2, and 1.7 mmol/l, at which the patients' awareness of and responses to hypoglycemia were evaluated. In the intervention group (n = 11), three short-term hypoglycemic ( < 2.2 mmol/l) episodes (days 1-3) preceded the first clamp study (day 4), whereas the second clamp study (day 6) followed a 2-day interval of strict avoidance of hypoglycemia. A control group (n = 5) was introduced to detect adaptation effects caused by the study procedure per se. RESULTS: This short-term avoidance of hypoglycemia caused improvement of the impaired counterregulatory hormone response during insulin-induced hypoglycemia involving adrenaline (P < 0.05), adrenocorticotrophic hormone (P < 0.03), and cortisol (P < 0.05). Improvement of hypoglycemia symptom awareness encompassed overall symptom perception (multiple analysis of variance, P < 0.04) and the automatic symptoms of heart pounding (P < 0.05) and sweating (P < 0.05). CONCLUSIONS: The previously reported compromised neuroendocrine counterregulation and symptom awareness, occurring as a consequence of repetitive hypoglycemic episodes over 2 days, may be improved by a single 2-day interval of strict avoidance of hypoglycemia

Recovery of hypoglycaemia-associated compromised cerebral function after a short interval of euglycaemia in insulin-dependent diabetic patients.

To test the hypothesis that compromised cerebral function, induced by recurrent hypoglycaemic episodes, may recover after a short interval of euglycaemia, we examined electrophysiological activity and symptom awareness during two sequential euglycaemic-hypoglycaemic clamp studies in 11 insulin-dependent diabetic patients without any signs of peripheral or autonomic neuropathy. Neurophysiological testing and evaluation of hypoglycaemic symptoms were performed at stable glycaemic plateaus of 5.6, 3.3, 2.2, and 1.7 mmol/l. The first clamp study was preceded by 3 short-term hypoglycaemic episodes, whereas the second clamp study followed a 2 day interval of strict euglycaemia. The latter caused a recovery of electrophysiological activity, which was demonstrated by recovery of delays of the middle latency auditory evoked potentials (latency shift of the P(a) component, MANOVA, P < 0.01). Reversal of hypoglycaemic symptom unawareness involved the overall symptom perception (MANOVA, P < 0.04), as well as the autonomic symptoms of heart pounding (P < 0.05) and sweating (P < 0.05). We conclude that the previously reported impaired cerebral function, occurring as a consequence of repetitive hypoglycaemic episodes, may recover after a single euglycaemic interval.