Early depressive symptoms after stroke: neuropsychological correlates and lesion characteristics

OBJECTIVE: To examine the relation between depressive symptoms and specific cognitive functions in patients with a recent stroke and to examine associations with lesion characteristics. METHODS: We studied 126 of 183 consecutive patients within 3 weeks after a first-ever symptomatic stroke (mean interval, 8.3+/-4.3 days). Presence and severity of depressive symptoms was assessed with the Montgomery Asberg Depression Rating Scale. Neuropsychological functioning was examined by means of a detailed neuropsychological examination covering six cognitive domains. We included a healthy control group (N=75) to obtain normative data for the neuropsychological examination. Functional impairment was measured with the modified Barthel Index and the modified Rankin Scale. Symptomatic and preexistent lesion characteristics were determined on CT or MRI. RESULTS: Of the included patients, 40% demonstrated mild and 12% moderate to severe depressive symptoms. Severity of depressive symptoms was related to lesion volume (p=0.008), functional impairment (all p<0.004), and degree of overall cognitive impairment (p=0.005). After adjustment for lesion size, a specific neuropsychological profile emerged in patients with moderate to severe depressive symptoms, affecting primarily memory, visual perception, and language (all p<0.05). No association was found between severity of depressive symptoms and lesion location, presence of preexistent lesions (white matter lesions and silent infarcts), and demographic factors (age, education, and gender). CONCLUSIONS: Moderate or severe symptoms of depression in the early stage poststroke are associated with a specific pattern of cognitive impairment, lesion size, and functional status. We suggest that depressive symptoms early after stroke are, at least in part, a reactive phenomenon secondary to severe cognitive and functional deficits.     

Migraine and TIAs; possibly more overlap than difference

Headache and transient neurological deficits can occur both in patients with migraine and in patients suffering a transient ischaemic attack (TIA). Consequently differentiating between these two disorders may be difficult. Recently, silent cerebral infarcts and ischaemic lesions in the subcortical white matter were found to be associated with migraine and in particular, with migraine with aura. The predominance of cerebellar infarcts in these patients is difficult to understand. Whether ischaemic damage in the brain of patients with migraine should be managed in a manner similar to that of patients with TIAs, should be the subject of future research.     

Treatment or prevention of complications of acute ischemic stroke

Both neurologic and medical complications influence outcome after stroke. Space-occupying supratentorial infarcts can cause transtentorial or uncal herniation, which leads to death. Treatments aimed at reducing intracranial pressure in patients with such infarcts are of unproven value. Mass-producing cerebellar infarction may lead to brainstem compression and obstructive hydrocephalus. These lesions often are treated surgically. Although anticonvulsants are not indicated for prophylaxis, the occurrence of epileptic seizures mandates treatment to prevent recurrences. Depression is common in the acute stage of stroke, but is probably not more prevalent after stroke than after myocardial infarction. Although dysphagia is common, it usually is a transient problem. Patients with a decrease of consciousness or brainstem dysfunction usually need tube feeding for a certain period of time. Medical complications, such as fever, infections, hyperglycemia, cardiac disorders, pressure sores, and deep venous thrombosis, are associated with a poor prognosis and should be treated as early as possible. Measures to prevent these complications are part of general care. Hypertension is very common during the week after stroke and should be treated only in case of extremely high values or malignant hypertension. A multidisciplinary approach in the stroke unit is necessary to prevent and manage complications in the acute phase of stroke.     

Cognitive impairment in patients with carotid artery occlusion and ipsilateral transient ischemic attacks

Abstract. Although transient ischemic attacks (TIAs) by definition do not cause lasting neurological deficits, cognitive impairment has been suggested in patients with carotid artery disease who have suffered from a TIA. The purpose of our study was to assess whether patients with carotid artery disease and TIAs are cognitively impaired, to describe the frequency, nature and severity of this impairment, and to search for associated patient characteristics.Thirty-nine consecutive patients with carotid occlusion and ipsilateral cerebral or retinal TIAs, and 46 healthy controls underwent extensive neuropsychological assessment. Performances were compared group-wise with analysis of variance. In addition, the presence of cognitive impairment in the individual patient was determined. Associations between illness characteristics and cognitive impairment were explored with regression analysis.Fifty-four percent of patients were cognitively impaired. Cognitive deficits were non-specific in nature and mild in severity. Impairment occurred also in patients with isolated retinal symptoms and in those without visible ischemic brain lesions on MRI. Neither the presence of any vascular risk factor, the side of the symptomatic carotid occlusion, the uni- or bilaterality of carotid occlusion, nor the number of cerebral ischemic lesions were predictors of cognitive impairment.We conclude that about half of the patients with carotid artery occlusion and ipsilateral TIAs are cognitively impaired. The presence of cognitive deficits in patients with isolated retinal symptoms and in those without cerebral ischemic lesions on MRI argues against an exclusive role for structural brain damage in the pathogenesis of these deficits.     

Cognitive functioning in patients with a small infarct in the brainstem.

Earlier findings in patients with a small supratentorial white matter infarct demonstrated subtle impairments of cognition. This is in line with reported difficulties in regaining premorbid level of functioning in daily life activities, even though any physical neurological deficits are no longer present. Either a "bystander effect" of adjoining gray matter or a long distance effect through hypometabolism or other neurochemical changes might underlie these impairments. To find the best explanation, a group of 17 patients with a lacunar infarct in the brainstem was neuropsychologically evaluated and compared with a closely matched control group. The patients demonstrated significantly impaired task performance on a constellation of neuropsychological tasks that was very similar to the findings previously found in patients with a supratentorial lacunar infarct (Boston Naming Test, TEA visual elevator, category fluency, Trailmaking Test). We conclude that a small white-matter infarct may affect cognitive functioning in a nonspecific way independently of its location.     

Dietary fat, body weight, and cancer: contributions of studies in rodents to understanding these cancer risk factors in humans

Understanding diet and energy balance as risk factors for breast, colon, and other cancers requires information on the contribution of each factor and of interactions among factors to cancer risk. Rodent models for breast cancer provide extensive data on effects of dietary fat and calories, energy balance, body weight gain, and physical activity on tumor development. Analyses of the combined data from many studies have shown clearly that quality and quantity of dietary fat and energy balance contribute independently to increased mammary gland tumorigenesis. These findings were seen in female rats fed diets high in fat (35-40% of calories) compared to rats fed control diets, with approximately 10% of calories as fat (Fay and Freedman, 1997, Breast Cancer Res. Treat. 46, 215-223). The methods used permit comparison of experimental and epidemiological data, and they may be useful in extrapolating between species and developing public health recommendations. In addition to the contributions of lifetime-diet composition, intake, energy balance, and physical activity to cancer risk, there are questions about the timing and duration of alterations in these factors and about the "dose-response" characteristics of cancer risk to the factors. Endocrine mechanisms may be significant in mammary gland tumor risk, but experimental and epidemiological data indicate that cancers at other sites, such as colon and liver, also are influenced by the factors listed. Other diet and lifestyle factors that influence energy, or specifically fat, metabolism may also affect risk for cancers that are promoted by increased intake of fat and calories. Studies of separate and interactive effects of dietary fat, black tea, weight gain, and mammary gland tumorigenesis (Rogers, et al, 1998, Carcinogenesis 19, 1269-1273) have been analyzed. Using adjustment of carcinogenesis endpoints for body weight, tumor burden, and latency, they were found to be related to weight gain within treatment groups in 2 of 3 experiments.      

The role of computed tomography in patients with lacunar stroke in the carotid territory

Summary In a prospective study of 78 patients presenting with recent clinical features of a supratentorially located lacunar infarct (LI), serial CT-scanning with contiguous 6, 5 or 3 mm slices was carried out. LI was found in 59 patients (76%; 95% confidence limits 65–85%). Lesions other than lacunar infarcts were found in 5 patients (6%; 95% confidence limits 2–14%); in only 14 patients could no abnormalities be detected (18%; 95% confidence limits 10–28%). There was no relationship between the detection rate on CT on the one hand and the type of lacunar syndrome, the number of previous TIA's, and the duration or severity of the neurological deficit on the other. A new protocol of CT-scanning for screening LI is advocated for situations where no MRI facilities are available or no patients cooperation can be obtained.     

Meniscal injuries: detection using MR imaging

Both retrospective and blinded analyses of thin-section, high-resolution magnetic resonance (MR) images of the knee joint, produced using a solenoid surface coil, indicate that MR imaging is an effective technique for evaluating meniscal injuries. Images of 49 patients were evaluated, and the results were correlated with those of subsequent arthroscopy. A grading scale was developed to rate the index of suspicion of a meniscal tear based on the MR images. Overall, approximately 80% of menisci rated grade 4 (definite tear) or 3 (probable tear) were found to have corresponding tears at arthroscopy. In many other patients with a grade 4 or 3 meniscus in whom a corresponding tear was not found arthroscopically, meniscal tears at other sites or other abnormalities were correctly diagnosed using MR. A majority of the false-positive MR images involved the posterior horns of the menisci, the sites of most false-negative arthroscopic diagnoses. The predictive value of a negative MR image was almost 100%. Even in patients with moderate-to-large effusions, the menisci were accurately evaluated. The results imply that MR imaging is useful in the preoperative evaluation of suspected meniscal tears.     

Chlorpropamide-induced pure white cell aplasia

We investigated the mechanism for isolated agranulocytosis and marrow pure white cell aplasia in an elderly man receiving 0.5 to 1.0 g per day of chlorpropamide (Chl) without other toxic drug exposure or overt systemic illness. Patient marrow revealed an absence of recognizable granulocytic precursors; megakaryocytes and erythroid precursors were normal. The WBC count was 1800/mm3 on admission with only 2% neutrophils; the absolute neutrophil count first exceeded 500/mm3 on the 17th day following cessation of Chl. A serum Chl level on admission was 100 micrograms/mL (acute phase, AP); no Chl was detected in serum (convalescent phase, CP) assessed on the 22nd hospital day. Antineutrophil antibodies were not detected, and T cell depletion failed to augment patient in vitro granulopoiesis. Patient AP serum produced potent complement-mediated inhibition (87% +/- 7%) of autologous granulocyte progenitors (CFU-GM) with minimal inhibition of erythroid (11% +/- 5%) or multipotent (5% +/- 4%) progenitor cells. Selective inhibition by patient AP serum of CFU-GM (74% +/- 11%) was also seen against two allogeneic marrows. Patient CP serum no longer inhibited (6% +/- 4%) autologous CFU-GM. Addition of Chl (5 to 120 micrograms/mL) to CP serum but not to control serum resulted in potent drug concentration-dependent complement-mediated inhibition of autologous and allogeneic CFU-GM. Inhibition of CFU-GM in the presence of Chl was no longer demonstrable following immunoabsorbent removal of IgG from patient serum. Patient serum in the presence of Chl had limited activity against morphologically recognizable marrow granulocytic precursors in a microimmunofluorescence assay. These results are most consistent with the development of Chl-dependent, selective antibody-mediated immune inhibition of granulopoiesis.