Daniel L. Labovitz

Depression but not seizure frequency predicts quality of life in treatment-resistant epilepsy

Background: The two-thirds of patients with epilepsy who become seizure-free have a quality of life (QOL) similar to the general population. The major treatment challenge is patients with refractory epilepsy. Whereas neurologists typically focus on seizure reduction in the treatment of these patients, results of studies relating seizure frequency to QOL are conflicting. As depression is associated with reduced QOL in epilepsy and antiepileptic medications (AEDs) can cause depression, it is important to determine the relative roles of depression and seizure frequency in QOL in refractory epilepsy. Methods: Prospective evaluation was conducted of patients with refractory epilepsy being admitted to an inpatient video-EEG monitoring unit. The impact of clinical variables (age, sex, marital status, seizure frequency, duration and type of seizure disorder, seizure localization, number of AEDs, depression) on QOL was analyzed. Results: Depression was a powerful predictor of QOL (n = 122, β = −35.8, p < 0.0001). No other variable predicted QOL. Depression was common (54%), severe (19% with suicidal thoughts), underdiagnosed (37%), and largely untreated (17% on antidepressants). Conclusions: Treatment of depression may be inadequately prioritized in the management of intractable epilepsy.

Prevalence and predictors of early seizure and status epilepticus after first stroke

Background: Early seizure (ES) has been reported in 2% to 6% of strokes and is a predictor of recurrent seizures. Acute stroke has been reported to cause 22% of all cases of status epilepticus in adults. The determinants of ES and status epilepticus (SE) after stroke, however, are not well understood. Methods: An incidence study was conducted to identify all cases of first stroke in adult residents of northern Manhattan. Cases of ES and SE within 7 days of stroke were identified through medical record review. Statistical analyses were performed using univariate and multivariate logistic regression models. Results: The cohort consisted of 904 patients; ES occurred in 37 (4.1%). The frequency of ES by stroke subtype and location was deep infarct 0.6% (2/356), lobar infarct 5.9% (20/341), deep intracerebral hemorrhage (ICH) 4.0% (4/101), lobar ICH 14.3% (7/49), and subarachnoid hemorrhage 8.0% (4/50). SE occurred in 10 patients (1.1%), representing 27.0% of patients with ES. Diabetes, hypertension, current smoking, alcohol use, age, gender, and race/ethnicity were not significant determinants of ES. In a subgroup of patients who had an NIH stroke scale (NIHSS) score recorded, NIHSS score was not an independent predictor of ES in multivariate analysis. After accounting for stroke severity, ES was not a predictor of 30-day case fatality. Conclusions: Lesion location and stroke subtype are strong determinants of ES risk, even after adjusting for stroke severity. ES does not predict 30-day mortality. SE occurs in more than one-quarter of patients with ES.

The incidence of deep and lobar intracerebral hemorrhage in whites, blacks, and Hispanics

Background: Black and Hispanic Americans have a greater risk of primary intracerebral hemorrhage (ICH) than whites. Deep ICH is most often associated with hypertension, while lobar ICH is associated with cerebral amyloid angiopathy. The authors conducted a population-based incidence study to directly compare the incidence of deep vs lobar ICH in all three race-ethnic groups. Methods: The authors used an active hospital and community surveillance program and autopsy reports to identify incident ICH cases among white, black, and Caribbean Hispanic adults in Northern Manhattan between July 1993 and June 1997. Incidence rates were adjusted for age and sex to the 1990 US Census. CIs for risk ratios (RR) were calculated with Byar’s χ2 approximation of the Poisson distribution. Results: The authors identified 155 cases of ICH for an annual incidence of 30.9/100,000 (26.7 to 35.0). Men had a higher risk of ICH than women (RR 1.5, 95% CI 1.2 to 1.8), driven entirely by the incidence of deep ICH (RR 1.8) rather than lobar ICH (RR 1.0). Compared with whites, RR for blacks was all ICH 3.8 (2.2 to 8.9), deep 4.8 (2.3 to 21.1), lobar 2.8 (1.2 to 14.4); RR for Hispanics was all 2.6 (1.4 to 6.1), deep 3.7 (1.7 to 16.5), lobar 1.4 (0.4 to 7.4). Conclusions: ICH is a heterogeneous disease with deep and lobar subtypes distinguishable on an epidemiologic basis. The different patterns of these two subtypes in our race-ethnically diverse population lend credence to the notion that ICH should no longer be treated as a single entity.

Incidence of adult brain arteriovenous malformation hemorrhage in a prospective population-based stroke survey

Background: Brain arteriovenous malformations (AVMs) represent a potential source of intracranial hemorrhage, especially in young adults, but prospective population-based incidence data on AVM hemorrhage are lacking. We investigated the incidence of first-ever AVM hemorrhage in adults based on population data from the Northern Manhattan Stroke Study (NOMASS). Methods: NOMASS is a prospective, population-based, stroke incidence survey collecting all hospitalized and nonhospitalized cases with first-ever (incident) stroke over the age of 20 in a ZIP code-defined area. All patients undergo CT and/or MR brain imaging and clinical data are systematically collected from the medical records. For this study, data on all cases with incident intracranial hemorrhage, i.e. any intracerebral, intraventricular and/or subarachnoid hemorrhage, occurring between July 1, 1993 and June 30, 1997 were used. Patients with intracranial hemorrhage due to trauma, tumor or intracranial vascular malformations other than a previously unknown AVM were excluded from the study. Results: Of the 207 patients diagnosed with a first-ever intracranial hemorrhage, 3 cases (1.4%) with an underlying brain AVM were identified. The crude incidence rate for first-ever AVM hemorrhage in our adult population was 0.55 per 100,000 person-years (95% confidence interval 0.11–1.61). Conclusions: Our results support prior findings from retrospective surveys. Population-based studies providing a prospective design for AVM detection and diagnosis are needed to confirm the data.

Spontaneous intracerebral haemorrhage

Spontaneous (non-traumatic) intracerebral haemorrhage accounts for at least 10% of all strokes in the United Kingdom,1 but the incidence is higher in some ethnic groups.w1 Intracerebral haemorrhage may present with a sudden focal neurological deficit or a reduced level of consciousness, after which it kills about half of those affected within one month and leaves most survivors disabled.2 Although early case fatality after spontaneous intracerebral haemorrhage has not changed over the past two decades,1 2 brain imaging has illuminated the pathophysiology of intracerebral haemorrhage and its various causes,3 w2 such that the term primary intracerebral haemorrhage now seems antiquated. Improving prevention of intracerebral haemorrhage in primary care and its outcome in secondary care is especially important in view of trends towards a rising incidence of intracerebral haemorrhage in an ageing population.1 No clinical scoring system has been shown to reliably differentiate intracerebral haemorrhage from ischaemic stroke.w3 Timely brain imaging is the key to recognising intracerebral haemorrhage. Computed tomography detects symptomatic intracerebral haemorrhage within minutes of symptom onset and up to one week thereafter; magnetic resonance imaging with gradient-recalled echo sequences reliably differentiates infarction from haemorrhage more than one week after onset of stroke.4 Diagnostic imaging distinguishes intracerebral haemorrhage from other types of intracranial haemorrhage (fig 1⇓), although intracerebral haemorrhage may extend into other intracranial compartments. This distinction is important, because the causes, prognosis, and treatment vary according to the location of intracranial haemorrhage.5 Fig 1 Axial illustration of the brain showing the subtypes of intracranial haemorrhage The major risk factors for spontaneous intracerebral haemorrhage are systemic arterial hypertension, excess alcohol consumption, male sex, increasing age, and smoking.6 w4 w5 These risk factors may lead to secondary vascular changes, such as small vessel disease and arterial aneurysms, which may eventually …

Subarachnoid hemorrhage incidence among whites, blacks and caribbean hispanics: The Northern Manhattan Study

American blacks and Hispanics may have a greater incidence of subarachnoid hemorrhage (SAH) than whites, but incidence data are scant. We used an active hospital and community surveillance program and autopsy reports to identify incident SAH cases among white, black and Hispanic adults living in Northern Manhattan between July 1993 and June 1997. The annual incidence adjusted for age and sex to the 1990 US Census was 9.7 per 100,000 (95% CI 7.5–12.0). Compared with whites (9 cases, age- and sex-adjusted annual incidence 8.2 per 100,000), the rate ratio of SAH was 1.3 (95% CI 0.7–2.4) for Hispanics (34 cases, incidence 10.9), and 1.6 (95% CI 0.8–2.8) for blacks (9 cases, incidence 12.8). The 30-day case fatality rate was 26%. Risk of death increased significantly with age and severity at onset but was not influenced by gender or race-ethnicity.

Intracerebral hemorrhage: update.

The present review focuses on evolving concepts in the pathogenesis and management of deep and lobar intracerebral hemorrhage subtypes, with particular focus on the relationship between lobar intracerebral hemorrhage, apolipoprotein E subtypes and cerebral amyloid angiopathy; deep intracerebral hemorrhage and the potential interaction between hypertension and low cholesterol; and new concepts in medical and surgical therapy for acute intracerebral hemorrhage.

Auras are frequent in idiopathic generalized epilepsy

The occurrence of an aura is often considered evidence of a partial rather than an idiopathic generalized epilepsy syndrome. The authors examined this hypothesis by prospectively recording reports of auras by patients being admitted for video-EEG monitoring. Auras were equally common (70%) among patients with idiopathic generalized epilepsy as they were among those with localization-related epilepsy. Presence of an aura is not a reliable indicator of localization-related epilepsy.

Lacunar infarct or deep intracerebral hemorrhage Who gets which? The Northern Manhattan Study

Lacunar infarcts (LACs) and deep intracerebral hemorrhages (DICHs) occur in the same structures and may result from the same pathology. It is unclear why one patient has an LAC while another has DICH. We compared LAC to DICH cases derived from a population-based incidence study. In multivariate analysis, LAC cases were significantly older, more likely to have diabetes, and had higher cholesterol than DICH cases.

Preventing stroke-related seizures When should anticonvulsant drugs be started?

Stroke is the leading cause of epilepsy after age 60.1 Despite the importance of the problem, there are few data on the natural history of stroke-related seizures and no good guideposts to suggest when to initiate anticonvulsant therapy after stroke. Can one identify stroke patients in whom one seizure is enough to justify lifetime anticonvulsant therapy? Does it make a difference whether the seizure occurs at stroke onset or months later? The stakes are high. Anticonvulsant drugs have many side effects and are often poorly tolerated in elderly patients. Since the risk for further seizures after a single unprovoked seizure is low, most epileptologists suggest starting anticonvulsant therapy only after a second seizure.2 However, for patients who have an unprovoked seizure after brain insult, the risk of a subsequent seizure is almost double that seen in patients with a seizure of unknown cause. Thus, the risk of epilepsy in some patients with …