Acute Ischemic Infarction Research Articles

Medial Vestibular Nucleus Lesions in Wallenberg's Syndrome Cause Decreased Activity of the Contralateral Vestibular Cortex

Three patients with the clinical diagnosis of Wallenberg's syndrome caused by acute unilateral ischemic infarctions, which included the vestibular nucleus in the medullary brain stem and afferent vestibular pathways, were examined by positron emission tomography (PET) during caloric vestibular stimulation. They all had typical signs of vestibular dysfunction such as transient rotatory vertigo with vomiting at the onset, ipsiversive body and ocular lateropulsion, and a complete ocular tilt reaction with tilts of the subjective visual vertical. Compared with healthy volunteers, who show activation in a network of temporoparietal vestibular areas within both hemispheres, especially in the posterior insula and retroinsular region that contains the human homologue of the parietoinsular vestibular cortex (PIVC) in monkeys, the activation pattern of the patients with Wallenberg's syndrome was typically changed. During caloric irrigation of the ear ipsilateral to the side of the lesion, they showed no or significantly reduced activation in the contralateral hemisphere, whereas the activation pattern in the ipsilateral hemisphere appeared "normal." These results are compatible with bilateral ascending vestibular pathways from the vestibular nuclei to the vestibular cortex. The novel finding in all three patients was that the activation patterns were compatible with the assumption that only the crossing fibers from the medial vestibular subnucleus to the contralateral medial longitudinal fascicle were affected, but the ipsilateral vestibular thalamocortical projections via the superior vestibular subnucleus were spared. Thus, the activation pattern in the PET study may reflect the vestibular tonic imbalance within the vestibular nuclei circuitry at the cortical level.

Effect of AMPA receptor antagonist YM872 on cerebral hematoma size and neurological recovery in the intracerebral hemorrhage rat model

[2,3-dioxo-7-(1 H-imidazol-1-yl)-6-nitro-1,2,3,4-tetrahydro-1-quinoxalinyl]-acetic acid monohydrate (YM872 or zonampanel), an AMPA receptor antagonist, is in clinical development for acute ischemic cerebral infarction. Stroke patients are prone to have subsequent intracerebral hemorrhages. In order to predict potential adverse effects, YM872 was tested in a rat model with collagenase-induced intracerebral hemorrhage. The morphologically determined hematoma volumes after 24 h were compared between animal groups intravenously infused with 3600 U/kg/h heparin for 30 min, or with 20 or 40 mg/kg/h of YM872, or placebo for 4 h. Heparin enlarged hematoma volume, but neither dose of YM872 affected hematoma size. In a separate study, neurological deficits were scored at various days after intracerebral hemorrhage induction in animals with intravenous infusion for 24 h of 10 or 20 mg/kg/h YM872, or saline. The YM872 groups scored significantly better than the saline group at 14 days. These data suggest that YM872 does not exacerbate intracerebral hemorrhage and might accelerate recovery.

Imaging tutorial: differential diagnosis of bright lesions on diffusion-weighted MR images.

High sensitivity (94%) and specificity (100%) have been reported in the diagnosis of acute cerebral infarction with diffusion-weighted magnetic resonance (MR) imaging. However, high signal intensity on diffusion-weighted MR images and low apparent diffusion coefficient values (similar to the findings in acute cerebral infarction) were reported in such diverse conditions as hemorrhage, abscess, lymphoma, and even Creutzfeldt-Jakob disease. The differential diagnosis of these conditions (eg, acute ischemic infarction and acute cerebral hemorrhage) is critical for the determination of appropriate treatment. The authors present a systematic review of bright lesions on diffusion-weighted MR images and their differential diagnosis, with emphasis on the practical and clinical approaches of differential diagnosis.

The Usefulness of Perfusion CT in Acute Cerebral Ischemic Infarction

The Usefulness of Perfusion CT in Acute Cerebral Ischemic Infarction

Diffusion MRI findings in isolated intracranial angiitis

This paper reports an 8-year-old girl with proven primary (isolated) angiitis of the central nervous system. On diffusion MRI, multiple scattered lesions were noted in the internal capsulas, thalami, and in the left middle cerebellar pedincle. These were hyperintense on b=1000 s/mm 2 (true diffusion) images. The apparent diffusion coefficient (ADC) values of these ranged between 0.40 and 0.52×10 −3 mm 2/s, consistent with acute ischemic infarction (cytotoxic edema). The ADC values of a relatively old lesion in the left occipital region ranged between 1.65 and 1.82×10 −3 mm 2/s, consistent with chronic infarction.

Painful alcoholic polyneuropathy with predominant small-fiber loss and normal thiamine status.

Although polyneuropathy related to chronic alcoholism has been reported frequently, its clinical features and pathogenesis remain to be clarified. To determine the clinicopathologic features and pathogenesis of alcoholic polyneuropathy associated with pain in patients with normal thiamine status, particularly in comparison to beriberi neuropathy. Clinical, electrophysiologic, and histopathologic findings were assessed in 18 patients with painful alcoholic polyneuropathy and normal thiamine status. Symmetric sensory-dominant polyneuropathy predominantly involving the lower limbs was the major clinical pattern. Painful sensations with or without burning quality represented the initial and major symptom. Progression of symptoms usually was gradual, continuing over months or years. Electrophysiologic and pathologic findings mainly indicated an axonal neuropathy. Densities of small myelinated fibers and unmyelinated fibers were more severely reduced than the density of large myelinated fibers, except in patients with a long history of neuropathic symptoms and marked axonal sprouting. The clinicopathologic features of painful symptoms and small axon loss are distinct from those of beriberi neuropathy. Sensory-dominant involvement with prominent neuropathic pain is characteristic of alcoholic neuropathy when thiamine deficiency is not involved, supporting the view of direct neurotoxic effect by alcohol or its metabolites.

A photothrombotic model of small early ischemic infarcts in the rat brain with histologic and MRI correlation

Over the last two decades several studies have suggested the role of photothrombotic occlusion of cerebral microvessels using rose bengal, resulting in small strokes in rodents that resemble those in humans. This paper describes such a photothrombotic method of acute small stroke induction in rats with histopathologic and in vivo magnetic resonance imaging (MRI) observations from 3 to 6 h after irradiation, which is homologous to a human autopsy specimen. Utilizing 30 min of irradiation with minimal beam intensity (0.1 W/cm 2) cold white light in conjunction with 20 mg of intravenous (iv) rose bengal as a rapid infusion, small infarcts were induced photochemically in the frontal lobes of six rats. The infarcts showed a consistent pattern on histologic and in vivo MR sections when examined within 7 h or less of irradiation. Both MRI and histologic sections were comprised of (a) a superior zone of infarcted neurons, (b) a middle curvilinear transition zone of edema on MRI and histologically vacuolated neuropil, and (c) an inferior zone of normal neurons. Shorter duration water-sensitive (T2)- and postgadolinium longer duration (T1)-weighted signal decay images both showed a curvilinear hyperintense transition zone of edema. The mean infarct and transition zone areas measured from the histologic sections were comparable to those measured on the MRI. The infarct model described above allows in vivo observations using MRI with the potential for use in testing putative neuroprotective agents. As demonstrated by a comparison with the histologic features of such infarcts in surgical and autopsy brain specimens, the model is relevant to acute human ischemic infarcts.

Use of exponential diffusion imaging to determine the age of ischemic infarcts.

Diffusion-weighted magnetic resonance imaging (DWI) detects acute ischemic infarcts with high lesion conspicuity. Determination of infarct age is difficult on DWI alone because infarct signal intensity (SIinfarct) on DWI is influenced by T2 properties ("T2 shine-through"). Maps of the apparent diffusion coefficient (ADC) reflect pure diffusion characteristics without T2 effects but have low lesion conspicuity. Thus, in clinical practice, combined use of DWI and ADC maps is required. Exponential DWI (eDWI) is an innovative means of MRI-diffusion data analysis that merges the advantages of DWI and ADC maps. The authors hypothesized that SIinfarct on eDWI would correlate with infarct age. The authors studied 114 consecutive patients who had 120 ischemic strokes with clearly determined onset times and who underwent echo-planar DWI. The eDWI were generated by dividing the signal intensity on DWI by that on the corresponding T2 image on a pixel-by-pixel basis. SIinfarct on eDWI was measured in the lesion core and expressed as a percentage of contralateral control tissue. On eDWI, relative SIinfarct changed significantly with infarct age (P < .0001). When patients were sorted in infarct-age groups, no significant differences were found within the first 120 hours. However, for patients studied within 5 days, the mean relative SIinfarct was significantly higher compared with patients studied > or = 8 days after stroke (P < .05). For all infarcts up to 5 days old, the eDWI signal intensity was higher than control tissue (hyperintense appearance). All infarcts > 10 days old had an eDWI signal intensity lower than control tissue (hypointense appearance). The authors concluded that the use of eDWI, as a single set of images, reliably differentiates acute infarcts (< or = 5 days old) from infarcts > 10 days old. This feature would be expected to be helpful when the distinction between acute and nonacute infarction cannot be determined on clinical grounds.

Diffusion-Weighted MR Imaging in Animal Model with Acute Ischemic Brain Infarction: Evaluation of Reversible Brain Injury

Purpose: To determine whether the analysis of abnormally high signal intensities in ischemic tissue, as revealed by diffusion-weighted MR imaging (DWI) can be used to evaluate reversible brain lesions in a cat model of acute ischemia. Materials and Methods: Ten cats were divided into two groups of five (Group I and Group II), and in all animals the middle cerebral artery was temporarily occluded. Group I underwent T2-DWI 30 minutes after occlusion, and Group II 120 minutes after occlusion. In both groups, DWI was performed one hour and 24 hours after reperfusion (at one hour, non-T2-weighted; at 24 hours, T2-weighted). Both occlusion and reperfusion were monitored by brain perfusion SPECT. All animals were sacrificed 24 hours later and their brain tissue was stained with TTC. Signal intensity ratios (SIR, signifying average signal intensity within the region of interest divided by that in the contralateral, nonischemic, homologous region) of the two groups, as seen on DWI were compared. The percentage of hemispheric lesions occurring in the two groups was also compared.Results: SIR after occlusion of the middle cerebral artery was 1.29 in Group I and 1.59 in Group II. Twenty-four hours after reperfusion, SIR in Group I was higher than in Group II (p

Superior mesenteric venous thrombosis in malrotation with chronic volvulus

Malrotation can be difficult to diagnose after the newborn period because of intermittent symptoms and vague clinical findings, but malrotation with midgut volvulus is usually quite striking in its presentation. Early diagnosis and surgical treatment are essential to prevent acute ischemic infarction of the bowel, although chronic complications are rare. The authors present an unusual case of mesenteric venous thrombosis secondary to chronic midgut volvulus. A 13-year-old girl presented with an 11-year history of recurrent bouts of abdominal pain evaluated at 3 other institutions without a diagnosis. At the referring hospital, an episode of bilious emesis associated with abdominal pain prompted a computerized tomography scan of the abdomen. This showed a calcified thrombus within the superior mesenteric vein (SMV). At laparotomy, malrotation with chronic 270° volvulus was found with evidence of mesenteric venous hypertension. Segmental occlusion was documented on magnetic resonance angiography. SMV thrombosis is an unusual complication of malrotation with chronic midgut volvulus. J Pediatr Surg 35:753-755. Copyright © 2000 by W.B. Saunders Company.

Perfusion MR Imaging in Patients with Acute Cerebral Infarction:Comparison with T2-Weighted and Diffusion-Weighted MR Imaging

Purpose: To evaluate the clinical usefulness of perfusion MR imaging by comparing with T2-weighted and diffusion weighted MR imaging in patients with acute cerebral ischemic infarction. Materials and Methods: Conventional, diffusion weighted, and perfusion MR images were obtained within one week of clinical onset in 14 cases of acute ischemic infarction. For perfusion MRI, the gradient-echo EPI technique after IV bolus injection of 15 cc of contrast media was used. Four kinds of perfusion MR images (rCBV, rCBF, mean transit time[MTT], time to peak concentration [TTP]) were generated by home-made software from the raw data. T2-weighted, diffusion-weighted, and perfusion images of each patient were retrospectively analyzed, with attention to the number, signal intensity, and size of lesions. Results: T2-weighted and diffusion-weighted images demonstrated 21 acute ischemic lesions in 14 patients. Six lesions had a long diameter of more than 3 cm, while the other 15 were smaller than 3 cm. On T2-weighted images, 17 lesions showed high signal intensity and four showed subtle high signal intensity. On diffusionweighted images, all lesions showed bright high signal intensity. The six lesions larger than 3 cm were all delineated by all four kinds of perfusion MR imaging, but among the 15 smaller than 3 cm, only four (26.7%), five (33.3%) and six (40%) were delineated on rCBV and rCBF maps, the MTT map, and the TTP map, respectively. As compared with T2-weighted and diffusion-weighted imaging, the rCBV and rCBF maps showed that four lesions were smaller and six were the same size. On the MTT map, three lesions were seen to be larger, four were smaller, and the other four were the same size as they appeared on diffusion-weighted images, while on the In TTP map, seven were larger and five were smaller than they appeared on these images. Conclusion: In all cases, diffusion-weighted images most clearly delineated acute ischemic lesions, regardless of lesion size. Many such lesions smaller than 3 cm were not apparent on perfusion MR images. Among the four kinds of perfusion MR imaging, TTP and MTT maps may be clinically useful for evaluation of the penumbral zone in cases of acute cerebral ischemic infarct.

Electrocardiographic manifestations: patterns that confound the EKG diagnosis of acute myocardial infarction—left bundle branch block, ventricular paced rhythm, and left ventricular hypertrophy

The 12-lead electrocardiogram (EKG), a powerful tool used in evaluating the chest pain patient, has its shortcomings. One such failing is encountered in a patient with one of the following electrocardiographic patterns: left bundle branch block (LBBB), ventricular paced rhythm (VPR), and left ventricular hypertrophy (LVH). These patterns reduce the ability of the EKG to detect acute coronary ischemic change and acute myocardial infarction (AMI). Several strategies are available to assist in the correct interpretation of these complicated electrocardiographic patterns, including a knowledge of the ST segment-T wave changes associated with these confounding patterns, performance of serial EKGs, and comparison with previous EKGs if available. This article suggests guidelines and interpretive tools for diagnosing AMI on EKG in patients with these confounding patterns.

T1 and magnetization transfer at 7 Tesla in acute ischemic infarct in the rat

T1 and magnetization transfer at a field strength of 7 Tesla were used to discriminate between water accumulation and protein mobilization in tissue undergoing infarction. Twelve rats subjected to acute stroke via intralumenal suture occlusion of the middle cerebral artery, and 19 controls, were studied. In MRI studies to 6 hr post-ictus, serial data acquisition allowed the measurement of cerebral blood flow (CBF), apparent diffusion coefficient of water (ADCw), equilibrium magnetization (M0) and T1, and equilibrium magnetization and T1 under an off-resonance partial saturation of the macromolecular pool (Msat and T1sat). Using these parameters, the apparent forward transfer rate of magnetization between the free water proton pool and the macromolecular proton pool, kfa, was calculated. Regions of interest (ROIs) were chosen using depressed areas in maps of the ADCw. T1 measurements in bovine serum albumin at 7T were not affected by the mobility of the macromolecular pool (P > 0.2), but magnetization transfer between free water and protein depended strongly on the mobility of the macromolecular pool (P < 0.001). For 6 hr after ictus, kfa uniformly and strongly decreased in the region of the infarct (P < 0.0001). Ratios (ischemic/non-ischemic) of parameters M0, Msat, T1, and T1sat all uniformly and strongly increased in the infarct. The ratio T1/T1sat in the region of infarction showed that a progressive accumulation of free water in the region of interest was the major (>80%) contribution to the decrease in kfa. There also existed a small contribution due to changes at the water-macromolecular interface, possibly due to proteolysis (P = 0.005). Magn Reson Med 41:696–705, 1999. © 1999 Wiley-Liss, Inc.

T1 and magnetization transfer at 7 Tesla in acute ischemic infarct in the rat.

T1 and magnetization transfer at a field strength of 7 Tesla were used to discriminate between water accumulation and protein mobilization in tissue undergoing infarction. Twelve rats subjected to acute stroke via intralumenal suture occlusion of the middle cerebral artery, and 19 controls, were studied. In MRI studies to 6 hr post-ictus, serial data acquisition allowed the measurement of cerebral blood flow (CBF), apparent diffusion coefficient of water (ADCw), equilibrium magnetization (M0) and T1, and equilibrium magnetization and T1 under an off-resonance partial saturation of the macromolecular pool (Msat and T1sat). Using these parameters, the apparent forward transfer rate of magnetization between the free water proton pool and the macromolecular proton pool, k(fa), was calculated. Regions of interest (ROIs) were chosen using depressed areas in maps of the ADCw. T1 measurements in bovine serum albumin at 7T were not affected by the mobility of the macromolecular pool (P > 0.2), but magnetization transfer between free water and protein depended strongly on the mobility of the macromolecular pool (P < 0.001). For 6 hr after ictus, k(fa) uniformly and strongly decreased in the region of the infarct (P < 0.0001). Ratios (ischemic/non-ischemic) of parameters M0, Msat, T1, and T1sat all uniformly and strongly increased in the infarct. The ratio T1/T1sat in the region of infarction showed that a progressive accumulation of free water in the region of interest was the major (>80%) contribution to the decrease in k(fa). There also existed a small contribution due to changes at the water-macromolecular interface, possibly due to proteolysis (P = 0.005).

The cerebral intravascular enhancement sign is not specific: a contrast-enhanced MRI study.

The intravascular enhancement (IVE) sign, also known as the "arterial enhancement sign", is an abnormal finding in the brain on contrast-enhanced MRI studies. IVE has been described in arterial cerebrovascular disorders, most commonly in acute or subacute arterial ischemic infarcts. However, the specificity of this sign has not been established. We describe four patients with disorders other than arterial strokes in whom gadolinium-enhanced high-field (1.5 T) MRI suggested IVE. The conditions were herpes simplex viral encephalitis, idiopathic cerebellitis, pneumococcal meningitis, and superior sagittal sinus thrombosis with venous infarction. IVE in these cases may be due to multiple factors, including arterial, venous, perivascular, and leptomeningeal or sulcal contrast medium accumulation. Our observations suggest that arterial ischemia, previously described as the cardinal cause of IVE, probably does not explain all instances, and urge caution in interpreting this sign as a specific MRI manifestation of acute arterial infarction or ischemia.

Integrin Polymorphisms as Risk Factors for Thrombosis

The study of integrin polymorphisms as risk factors for thrombosis is in its infancy. Like many other purported genetic risk factors, controversies abound, and it will take much work to shift through the information and identify those individuals for whom these genetic variations are true risks for thrombosis. There is a clear need for well-designed, large, prospective, genetic epidemiologic studies. Large clinical trials should be helpful in this regard, and genotyping patients in these studies will be the only way to correlate response to therapy with genetic factors (pharmacogenetics). Hand-in-hand with such clinical investigations, in vitro studies of the functional consequences of these inherited traits should provide a sound rationale for future interventions that will ultimately be beneficial to patients.

Superselective Intra-arterial Fibrinolysis for Acute Cerebral Ischemic Infarct: Usefulness of Diffusion Weighted MR Imaging1

Purpose : To evaluate the efficacy of superselective intra-arterial fibrinolysis for acute cerebral stroke and the usefulness of pre- and postfibrinolysis diffusion-weighted MRI (DWI). Materials and Methods : In 41 patients with acute ischemic stroke whose treatment involved intra-arterial fibri-nolysis, the occlusion site, degree of recanalization, and clinical results were compared. In 12 patients, diffu-sion weighted MRI was performed before fibrinolysis, and eight of these also underwent diffusion-weighted MRI after fibrinolysis. Using diffusion-weighted MRI, neurological outcomes were compared with signal in-tensity ratio (SIR, or the average signal intensity within the region of interest divided by that in the contralater-al, nonischemic, homologous region). Results : Twenty patients showed complete recanalization, nine partial recanalization, and in twelve there was no recanalization. Fourteen patients (34 %) improved neurologically. No relationship existed between occlu-sion sites, degree of recanalization, and clinical outcome. Among 12 patients who underwent DWI before fibrinolysis, complete recanalization was noted in eight. Neurological improvement was seen in four patients with low SIR(〈1.55),while in four with high SIR(〉1.7 ), neurological outcome was poor despite complete recanalization. Conclusion : Although superselective intra-arterial fibrinolysis for acute cerebral stroke is a good therapeutic method for recanalization, the clinical outcome can be disappointing. We therefore suggest that in cases of acute cerebral ischemic infaret, SIR-as seen on DWI-might be useful for predicting the benefits of recanaliza-tion. In such cases, further investigation of the use of DWI prior to fibrinolysis is therefore needed

The influence of delayed postischemic hyperthermia following transient focal ischemia: alterations of gene expression.

We have recently shown that moderate hyperthermia, even if delayed, markedly enlarges the volume of an acute ischemic infarct. In the current study, we used in situ hybridization autoradiography to assess the effects of delayed hyperthermia on the regional expression of messenger RNA (mRNA) for the immediate early genes c-fos and c-jun, the inducible heat-shock protein 70 (hsp70) and glial fibrillary acid protein (GFAP) following 1 h of transient middle cerebral artery occlusion (MCAo) produced in rats by the insertion of an intraluminal suture. Sham-occluded rats were also studied. One day after MCAo, rats were placed into a heating chamber, where cranial temperature was either maintained at 37-38 degrees C (normothermic group) or was elevated to 40 degrees C (hyperthermic group) for 3 h. At either 2 or 24 h thereafter, brains were studied by in situ hybridization. Low-level constitutive c-fos and c-jun expression in sham-occluded rats was unaffected by delayed temperature manipulation. Prior MCAo decreased c-fos and c-jun mRNA in the affected striatum and overlying cortex. In rats studied 2 h after delayed hyperthermia, however, c-fos mRNA was markedly increased in ipsilateral cingulate cortex. By contrast, the pattern of c-jun mRNA was similar in rats with prior MCAo irrespective of delayed normothermia or hyperthermia: increased expression involved ipsilateral cingulate and paramedian cortical areas. Bilateral increases in hsp70 expression were produced by hyperthermia alone, and hsp70 mRNA was densely increased throughout the ischemic cortex and striatum following MCAo, while delayed hyperthermia altered this pattern by extending the zone of increased hsp70 message to cingulate and paramedian cortical areas at 2 h. GFAP mRNA was decreased within the previously ischemic field but increased in surrounding regions. The induction of c-fos and hsp70 message in tissue regions abutting zones of enhanced injury in brains with delayed postischemic hyperthermia indicates that these zones have been additionally stressed: these gene responses may possibly contribute to the protection of these threatened regions.

Prevention of carotid artery thrombosis by oral platelet GPIIb/IIIa antagonist in dogs.

Current antithrombotic therapy in acute ischemic stroke and myocardial infarction in which a combination of antiplatelet agents (aspirin) and anticoagulants (heparin) was used led to partial reduction of acute thrombotic complications. Recent advances in antiplatelet research led to the discovery of the platelet glycoprotein IIb/IIIa complex (GPIIb/IIIa), the final common pathway for platelet aggregation. The present study was undertaken to determine the oral antithrombotic efficacy of a potent and specific platelet GPIIb/ IIIa antagonist, DMP728, in an electrically induced carotid artery thrombosis model in dogs. Based on the powerful antiplatelet efficacy of this mechanism in inhibiting all agonist-induced platelet aggregation as well as in inhibiting platelet procoagulant activity (thrombin generation and hence fibrin formation), an orally active antagonist for this integrin receptor might have potential benefits in stroke. Anesthetized dogs were instrumented for monitoring of arterial blood pressure, heart rate, and carotid artery flow velocity. Animals were treated with saline or DMP728 (0.1 to 1.0 mg/kg PO). Thrombus formation (platelet-rich aggregate with fibrous coating and a few erythrocytes) by anodal electrolytic stimulation (300 microA) to the intimal surface of the right carotid artery was initiated 120 minutes after oral DMP728 administration and continued for 180 minutes. Whole blood cell counts, ex vivo platelet aggregation, and template bleeding time were determined at different time points throughout the study. DMP728 administered at 0.1 to 1.0 mg/kg PO exhibited dose-dependent antithrombotic efficacy in this model. DMP728 was shown to be significantly effective in inhibiting ex vivo platelet aggregation and in inhibiting thrombosis at 0.3 to 1.0 mg/kg PO. The antiplatelet, antithrombotic effects of DMP728 were demonstrated without any significant changes in the different hemodynamic or coagulation parameters. These data demonstrated the oral antithrombotic efficacy of DMP728 in dogs. Platelet GPIIb/IIIa blockade with an orally active antagonist was shown to be safe and effective in the prevention of carotid artery occlusive thrombosis.

Profile of a Neurology Residency

The pattern and frequency of patient encounters during the Boston (Mass) University adult neurology residency program (1988 to 1991) for one resident was compared with that in general neurology practice as well as with the frequency of neurologic disorders in the US population. A total of 1332 new patients (85% adult, 15% pediatric) were seen during a 3-year period. This total represented 970 inpatients (73% of all patients) and 362 outpatients (27%). The resident encountered more patients in the hospital (7.5 admissions or 13 consultations per week) and fewer patients in the clinic (2.5 new outpatients per week) than does the average community neurologist (two admissions, 8.7 consultations, and 13.2 new outpatients). The most common diagnosis for an admission encounter was acute ischemic infarct; for a consultation, metabolic encephalopathy; and for an outpatient encounter, radiculopathy. Less prevalent neurologic disorders in the United States (eg, cognitive, demyelinating, movement, and neoplastic disorders) were encountered more frequently in residency than were very prevalent neurologic disorders (eg, headache and trauma). This is the first reported summary of all patients one resident actually encountered during neurology training. The patient encounter profile suggests that this residency training overemphasized acute inpatient care of less prevalent neurologic disorders compared with outpatient care of more prevalent disorders commonly seen in a neurology practice. Accumulation of similar data from other residencies and practicing neurologists can help residency directors assess the changing needs of residents in training and guide curriculum in response to changes in practice patterns.