Carotid endarterectomy in the elderly.

BACKGROUND AND PURPOSE: Increasing life expectancy has resulted in an increasing number of elderly. As the elderly population grows, the incidence of stroke will increase. Many such strokes result from carotid stenosis (CS). In view of the benefits of carotid endarterectomy (CEA) shown in recent clinical trials, it would seem prudent that surgery for CS be considered for prevention of stroke in this population. Traditionally, members of the geriatric population have often been viewed, perhaps arbitrarily, as inappropriate candidates for CEA because of perceived greater operative risks. The purpose of this study was to assess the safety of performing CEA in geriatric patients. PATIENTS AND METHODS: A total of 175 patients who underwent CEA between January 1994 and June 1996 were evaluated retrospectively. The patients were divided into the nongeriatric group (NGG <75 years of age) and the geriatric group (GG >75 years of age). There were 90 (51%) patients in the NGG and 85 (49%) in the GG. The two groups were compared for the following: rationale for surgery (symptomatic vs. asymptomatic), risk factor profile, preoperative imaging studies (noninvasive vs. invasive), and complications of surgery. RESULTS: Both groups were generally comparable in terms of their risk factors, rationale for surgery, and preoperative cardiac risk. Noninvasive imaging alone was used in 56% of NGG and 60% of GG patients, whereas 44% of NGG and 40% of GG underwent invasive cerebral angiography in addition to other noninvasive studies. There were 4(4.4%) postoperative neurological complications, including two strokes and two transient ischemic attacks (TIAs), in the NGG and 1(1%) stroke in the GG. One patient died in the NGG from a stroke. Although one patient in the GG experienced a postoperative myocardial infarction, there was no mortality in this group. CONCLUSION: CEA can be safely performed for both symptomatic and asymptomatic CS in appropriately selected patients irrespective of age.

Amlodipine for migraine prophylaxis.

Migraine is among the most common neurologic disorders encountered in clinical practice. In the general US population, the annual incidence has been calculated to be approximately 250 per 100,000 with a point prevalence of 10%. Females are affected more than males. A variety of prophylactic and abortive medications are being used for treatment and several are being studied in clinical trials. Calcium-channel blockers are frequently used prophylactic medications. We report two patients with migraine successfully treated with amlodipine (Norvasc, Pfizer, Inc), a slow calcium-channel blocker. To our knowledge, these are the first reported cases of amlodipine used in migraine prophylaxis.

Acute leukocyte and temperature response in hypertensive intracerebral hemorrhage.

BACKGROUND AND PURPOSE: We undertook this study to investigate the relationship between outcome, hematoma volume, and admission peripheral white blood cell count and body temperature in acute hypertensive intracerebral hemorrhage. METHODS: Eighty-two consecutive patients who presented with hypertensive intracerebral hemorrhage within 72 hours of onset were retrospectively assessed. The peripheral white blood cell count, polymorphonuclear leukocytes, and the body temperature on admission were measured. The outcome at 30 days after ictus was determined with a modified Glasgow Outcome Scale. Correlation analysis was performed between these measurements and hematoma volume, which was calculated by brain computed tomography. We also looked at the presence or absence of intraventricular extension. RESULTS: The mean hematoma volume was significantly greater in those patients who died compared with those with a good, moderate, and severe outcome (79.6 cm3 versus 10.7, 18.3, and 19.9 cm3, respectively; P < .0005). The mean peripheral white blood cell count was higher in those who died than in the other three groups (12.580 +/- 0.521 versus 8.160 +/- 0.543, 8.565 +/- 0.543, and 7.427 +/- 0.786 x 10(9)/L, respectively; P < .0005). The mean body temperature of those who died tended to be higher than those in the good-outcome group (99.12 +/- 0.21 versus 98.18 +/- 0.21 degrees F, P < .05). A positive linear correlation was observed between hematoma volume and white blood cell count (r = .506, df = 77, P < .001), as well as the polymorphonuclear leukocyte count (r = .561, df = 76, P < .001). A trend was also observed for admission temperature (r = .265, df = 74, P < .05). The leukocyte response was enhanced by the presence of intraventricular extension. CONCLUSIONS: There is a relationship between the size of the hematoma and the degree of leukocytosis in hypertensive intracerebral hemorrhage. This relationship appears to most likely represent a stress-induced reaction of the white blood cell count.

Relation between blood pressure and outcome in intracerebral hemorrhage.

BACKGROUND AND PURPOSE: Controversy continues to exist regarding optimal blood pressure control in acute hypertensive intracerebral hemorrhage. Persistent marked elevation of the blood pressure can promote further bleeding, increase cerebral blood flow, and raise intracranial pressure. Relative hypotension, on the other hand, may promote hypoperfusion with secondary ischemia. This study was designed to assess outcome in patient groups defined by the degree of elevation in their pretreatment and posttreatment blood pressures. METHODS: We retrospectively assessed 87 patients who were categorized according to an initial mean arterial pressure > 145 mm Hg (n = 34) compared with those with a pressure < or = 145 mm Hg (n = 53). We also studied blood pressure control within the first 2 to 6 hours of presentation with subjects categorized according to a mean arterial pressure > 125 mm Hg (n = 40) or < or = 125 mm Hg (n = 47). RESULTS: An improved outcome in both mortality and severe morbidity was observed in the < or = 145 (chi 2 = 7.0, P < .005) and the < or = 125 mm Hg (chi 2 = 6.7, P < .005) groups. CONCLUSIONS: Markedly elevated blood pressure on admission and persistent inadequate blood pressure control adversely affect the prognosis in hypertensive intracerebral hemorrhage.

MRI of AIDS-related polyradiculomyelitis.

OBJECTIVE: We describe the unusual syndrome of cytomegalovirus (CMV) polyradiculomyelitis and its MR findings in two patients with AIDS. MATERIALS AND METHODS: The clinical records and MRI studies of two patients with AIDS and CMV polyradiculomyelitis were reviewed. The MR images were performed on a Picker 1.0 or 1.5 T MR unit. Axial and sagittal T1-weighted images of the lumbar spine were obtained, pre- and post-Gd-DTPA (0.1 mmol/kg) administration. Gradient echo sagittal images were also obtained. RESULTS: Precontrast images demonstrated a thickened cauda equina in both patients. In one patient the conus was ill defined on precontrast images. Post-contrast images demonstrated diffuse enhancement of the cauda equina in both patients as well as enhancement along the surface of the conus. In one patient the nerve roots were clumped and adherent to the walls of the thecal sac as well as to other nerve roots. CONCLUSION: The clinical presentation of urinary retention, flaccid paraparesis, back and/or leg pain, and "saddle anesthesia" in a patient with AIDS should suggest the diagnosis of CMV polyradiculomyelitis. Although diffuse enhancement of the cauda equina on postcontrast MRI is a nonspecific finding, it would strongly support this diagnosis in the appropriate clinical setting. The diagnosis may be easily missed without the use of a contrast agent.

Potential environmental neurotoxins related to 1-methyl-4-phenylpyridinium: selective toxicity of 1-methyl-4-(4'-acetamidophenyl)-pyridinium and 1-methyl-4-cyclohexylpyridinium for dopaminergic neurons in culture.

Mesencephalic cells in culture were exposed to various compounds which we hypothesized to be selective toxins for dopaminergic neurons. The culture system was previously shown suitable for assessing selective dopaminergic neurotoxicity, since 1-methyl-4-phenyl-pyridinium (MPP+), the active metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridinium, destroyed dopaminergic neurons without affecting other cells. Some compounds tested were selected to fulfill two criteria believed to underly the selective dopaminergic neurotoxicity of MPP+, i.e., to be a potential substrate for the uptake carrier for dopamine and to possess a strong delocalized positive charge to inhibit the mitochondrial respiratory system. Other compounds were chosen on the basis of clinical or anecdotal evidence linking them to Parkinson's disease. Among the tested compounds two pyridinium analogs, 1-methyl-4-(4'-acetamidophenyl)pyridinium (MACPP+) and 1-methyl-4-cyclohexylpyridinium (MCP+) were found to be selectively toxic toward dopaminergic neurons. Incubation of cultures with both MACPP+ and MCP+ produced a dramatic reduction in the number of tyrosine hydroxylase-positive cells and the uptake of [3H]dopamine without reducing the number of cells visualized by phase-contrast microscopy or the uptake of [3H]aminobutyric acid. Besides MACPP+ and MCP+ none of the tested compounds exhibited any selective dopaminergic neurotoxicity. Together with earlier findings, these data suggest that the structural requirements are rather strict for a chemical to be a selective dopaminergic neurotoxin and make it unlikely that there is a wide spectrum of environmental dopaminergic toxins.

Toxicity of 1-methyl-4-phenylpyridinium for rat dopaminergic neurons in culture: selectivity and irreversibility.

Cultures of dissociated embryonic rat mesencephalic cells were exposed to 10 microM 1-methyl-4-phenylpyridinium (MPP+), a concentration shown earlier to result in loss of greater than 85% of tyrosine hydroxylase (TH)-positive neurons without affecting the total number of cells observed by phase-contrast microscopy. To characterize better the selectivity of the toxic action of MPP+, other parameters were measured reflecting survival and function of dopaminergic or nondopaminergic neurons. Exposure of cultures to 10 microM MPP+ for 48 h reduced TH activity to 11% of control values without reducing protein levels. [3H]Dopamine uptake was reduced to less than 4% of control values, whereas the uptake of gamma-[3H]aminobutyric acid ([3H]GABA) was not affected in these cultures. This same treatment failed to reduce the number of cholinergic cells visualized in septal cultures and did not affect either choline acetyltransferase activity or high-affinity choline uptake. To assess for possible recovery of dopaminergic neurons, cultures were exposed to 10, 1.0, or 0.1 microM MPP+ for 48 h and then kept for up to 6 days in MPP(+)-free medium. After exposure to 10 microM MPP+, the number of TH-positive neurons, their neurite density, TH activity, and [3H]dopamine uptake remained at constant, reduced levels throughout the period of observation after termination of exposure, whereas GABA uptake remained normal. Treatment with lower concentrations of MPP+, i.e., 1.0 and 0.1 microM, induced less pronounced dopaminergic toxic effects. However, no recovery was seen after posttreatment incubation in toxin-free medium. These findings provide evidence that MPP+ treatment results in highly selective and irreversible toxicity for cultured dopaminergic neurons.

Toxic effects of potential environmental neurotoxins related to 1-methyl-4-phenylpyridinium on cultured rat dopaminergic neurons.

Dopaminergic rat mesencephalic neurons in culture were exposed to a group of potential environmental neurotoxins. These cultures, which contained 0.5 to 1% dopaminergic neurons, were a suitable tool for determining nonselective and selective dopaminergic cytotoxicity. Selective toxicity was quantitated as the concentration which destroyed half of the population of dopaminergic neurons as visualized by tyrosine hydroxylase immunocytochemistry. Nonselective toxicity was defined as the concentration of test drug which destroyed half of the entire population of cultured cells as visualized by phase contrast microscopy. The compounds tested were selected to fulfill two molecular criteria underlying the toxic activity of 1-methyl-4-phenylpyridinium (MPP+), the active metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine toward dopaminergic cells: 1) to be a substrate for the selective uptake system of the dopaminergic neurons and 2) to possess a delocalized positive charge related to their ability to inhibit mitochondrial electron transport. Of a total number of 29 compounds tested, MPP+ and its close derivatives, 2'-methyl-MPP+ and p-amino-MPP+, exhibited highly selective dopaminergic toxicity, hence the requirements for a selective dopaminergic neurotoxin are rather strict.