United Arab Emirates (UAE) population is growing and it is to reach 13,163,548 by 2050 and it is mainly composed of expatriates - only 11% are UAE Nationals (UAEN). The epidemiological stroke data for UAE is limited especially in young patients. We studied all young ischemic stroke patients (YISP; 50 years cut off) admitted to Cleveland Clinic Abu Dhabi (CCAD) from May 2015 till May 2018. We studied demographics, risk factors, TOAST classification and outcomes. We used descriptive statistics and student t test for continuous variables; statistical significance was at 0.05. There were 146 YISP: (mean age 40.3 y; min 22, max 50), there were 42 women (28.8%) and 104 men (71.2%); there was no age difference between the two (40.5 vs. 40.2; p=ns); there were 48 UAEN (32.9%) and 98 expats (67.1%) and there was no age difference between the two (40.7 vs. 40; p=ns). The most common risk factor was dyslipidemia (73.3%) followed by hypertension (63%), diabetes (39.7%), obesity (34.2%), smoking (23.3%), ischemic heart disease (9.6%). There were 25.3% large artery strokes, 22.6% cardioembolic, 19.9% undetermined, 17.8% small vessel and 14.4% other etiologies. Initial mean NIHSS score was 9.49 (range 0-39); 16.4% of patients had mRS 0-1at discharge, case fatality was 3.4%. Our data show high prevalence of dyslipidemia and hypertension in YISP. There was high frequency of large artery and cardioembolic strokes. Minority of YISP had favorable outcome at discharge. Prospective studies are needed to further elucidate stroke epidemiology and prognosis in UAE especially in young patients.
BACKGROUND:Surgery for intracranial aneurysm often results in postoperative neurologic deficits. We conducted a randomized trial at 30 centers to determine whether intraoperative cooling during open craniotomy would improve the outcome among patients with acute aneurysmal subarachnoid hemorrhage. METHODS:A total of 1001 patients with a preoperative World Federation of Neurological Surgeons score of I, II, or III ("good-grade patients"), who had had a subarachnoid hemorrhage no more than 14 days before planned surgical aneurysm clipping, were randomly assigned to intraoperative hypothermia (target temperature, 33 degrees C, with the use of surface cooling techniques) or normothermia (target temperature, 36.5 degrees C). Patients were followed closely postoperatively and examined approximately 90 days after surgery, at which time a Glasgow Outcome Score was assigned. RESULTS:There were no significant differences between the group assigned to intraoperative hypothermia and the group assigned to normothermia in the duration of stay in the intensive care unit, the total length of hospitalization, the rates of death at follow-up (6 percent in both groups), or the destination at discharge (home or another hospital, among surviving patients). At the final follow-up, 329 of 499 patients in the hypothermia group had a Glasgow Outcome Score of 1 (good outcome), as compared with 314 of 501 patients in the normothermia group (66 percent vs. 63 percent; odds ratio, 1.14; 95 percent confidence interval, 0.88 to 1.48; P=0.32). Postoperative bacteremia was more common in the hypothermia group than in the normothermia group (5 percent vs. 3 percent, P=0.05). CONCLUSIONS:Intraoperative hypothermia did not improve the neurologic outcome after craniotomy among good-grade patients with aneurysmal subarachnoid hemorrhage.
Wind-up, a manifestation of nociceptive system plasticity, refers to the incremental increase in the magnitude of evoked responses at the level of the dorsal horn or the trigeminal nucleus caudalis in response to persistent c-nociceptor input. Wind-up clinically manifests as 1)temporal summation of repetitive noxious stimuli, and 2) prolongation of second pain, the delayed burning component that follows the initial acute sharp sensation of nociceptive pain (aftersensations). While not identical to central sensitization, wind-up is the likely clinical precursor to the development of central sensitization (allodynia and hyperpathia) in humans. By adapting an electronic von Frey filament, we have developed a device for delivering reproducible mechanical noxious stimuli to the trigeminal dermatomes. In this way we have been able to measure psychophysical markers of central sensitization and wind-up in patients with headaches and facial pain syndromes. Using a paradigm of variable load, fixed frequency (0.8 hz) mechanical stimulation of bilateral V1 dermatomes, we induced repetitive noxious stimuli and measured the presence of temporal summation of second pain and the duration of aftersensations in both chronic headache patients and age-matched controls. We retested the patients using the same paradigm after detoxification and successful treatment of their headaches. Preliminary results show that 1) analgesic-induced chronic headaches have prolonged aftersensations compared with controls and headache resolution consistently leads to a reduction of aftersensation duration anywhere between 35–95% of pretreatment values; 2) chronic headache patients exhibiting temporal summation display significantly greater prolongation of aftersensations than those without it, and; 3) allodynia resolves in all successfully treated patients. We conclude: 1) this device measures psychophysical markers of wind-up and central sensitization; 2) aftersensations may be a useful marker of central neuronal hypersensitivity of the nociceptive pathways; and 3) resolution of analgesic-induced chronic headache is accompanied by reduction in the duration of aftersensations.
Objectives.-To describe the occurrence of cerebral venous thrombosis in a 40-year-old man whose cerebral event was induced by a poor golf swing, to review the literature on possible mechanisms producing venous thrombosis, and to compare this case with the literature.Background.-Headache is the most frequent symptom in patients with cerebral venous thrombosis. However, patients presenting with a headache due to cerebral venous thrombosis are uncommon. The known risk factors for thrombosis include both acquired and genetic factors. When the interaction of these two groups occurs, the magnitude of this interaction is thought to produce a dynamic state that can favor thrombosis. Our case report illustrates that moderate levels of anticardiolipin antibodies together with the mild trauma of a golf swing can induce a cerebral venous thrombosis. This case also suggests that although headache is rarely due to cerebral venous thrombosis, it should be excluded by good medical acumen and testing.Results.-Minor trauma induced by a poor golf swing was chronologically related to the development of a progressive cerebral venous thrombosis. The patient had none of the risk factors associated with a predisposition to venous thrombosis: hypercoagulable state, concurrent infection, pregnancy/puerperium, collagen vascular disorder, malignancy, migraine, false-positive VDRL, previous deep vein thrombosis, renal disease, factor V Leiden, or a hematological disorder. There was no anatomical abnormality that would predispose the patient to a cerebral venous thrombosis. The only laboratory abnormality was a moderate anticardiolipin antibody level (25 GPL). The patient was placed on warfarin sodium therapy and is currently without clinical sequela from the venous thrombotic event.Conclusions.-Under certain circumstances, minor trauma can induce cerebral venous thrombosis. A review of the literature indicates that cerebral venous thrombosis in the presence of anticardiolipin antibodies and in the absence of systemic lupus erythematosus is a rare event. Previously, only major traumatic events have been reported to be associated with cerebral venous thromboses. The chronological development of cerebral venous thrombosis after a faulty golf swing strongly indicates that given a background of moderate levels of anticardiolipin antibodies, even minor trauma can induce a venous thrombotic event.