Proximal Left Middle Cerebral Artery Research Articles

Abstract Number ‐ 66: Symptomatic Chronic Internal Carotid Artery Occlusion Managed With Bilateral Common Carotid Angioplasty: A Case Report

Introduction Several guidelines have addressed symptomatic or asymptomatic carotid artery stenosis treatment with intensive medical management and surgical management based on the severity of stenosis [1]. In acute occlusions, endovascular treatment (EVT) and carotid endarterectomy (CEA) with or without prior thrombolytics provide the best recanalization and functional outcomes when compared to intravenous or intra‐arterial thrombolysis alone. There is, however, less robust evidence on management of symptomatic chronic internal carotid artery (ICA) occlusion occurring in tandem with significant contralateral ICA stenosis [2]. In chronic ICA occlusion (ICAO), EVT and carotid endarterectomy (CEA) are technically unfeasible, but indirect procedures have been arising as safe and effective alternatives, notably CEA or stenting of contralateral stenotic ICA [3] and CEA or stenting of ipsilateral external carotid artery (ECA) [4]. We hereby report a case of symptomatic chronic ICAO that was managed with staggered angioplasty and stenting of bilateral common carotid artery (CCA) bifurcations. Methods We hereby present a case report. Results A 62‐year‐old male with atrial fibrillation and hypertension woke up with sudden dysarthria and right upper extremity and facial weakness. NIHSS at presentation was 4. Last seen normal 9 hours prior. Non‐contrast head computerized tomography (CT) did not show acute intracranial abnormality, CT angiogram of head and neck showed severe right ICA stenosis and complete occlusion of the left ICA at cervical, petrous and cavernous segments, with distal reconstitution at the supraclinoid segment with left proximal middle cerebral artery (MCA) thrombus. CT perfusion showed a core infarct volume of 8cc in left MCA territory, mismatch volume of 78cc and ratio of 10.8. Risks of acute neuro‐intervention were deemed to outweigh benefits. Given favorable perfusion imaging, and in concordance with the EXTEND trial [5], tPA was administered. The patient remained stable without hemorrhagic complications with residual deficits of mild right upper extremity weakness and mild expressive aphasia. MRI confirmed left ICA territory ischemic infarcts. Patient underwent stenting of the asymptomatic right ICA at the CCA bifurcation first, followed by left CCA stent after one month with impressive improvement in subsequent perfusion imaging. Conclusions Our case encourages consideration of well‐timed angioplasty and stenting in cases of chronic bilateral carotid artery disease especially when the asymptomatic side is also significantly stenotic

Abstract 1122‐000021: Delayed Vasospasm and Cerebral Ischemia Following Mild Traumatic Brain Injury

Introduction : Post‐traumatic vasospasm (PTV) is a significant cause of morbidity and mortality following traumatic brain injury (TBI). 1 Delayed PTV is thought to occur due to inflammation from SAH. 1 The risk of symptomatic PTV is associated with the severity of TBI. 1,2,3 Treatment of PTV traditionally involves agents used in aneurysmal vasospasm such as Nimodipine. Intra‐arterial and intravenous verapamil and milrinone have been utilized to treat PTV. 4 We present a rare case of delayed cerebral ischemia caused by PTV without SAH treated with intra‐arterial milrinone and oral verapamil. Methods : This is a case report of a case of a 16‐day delay of cerebral ischemia secondary to PTV. Results : A 19‐year‐old female without significant medical history presented to the emergency room as the restrained driver in a motor vehicle collision involving a car versus a tree. The patient’s Glasgow Coma Scale score was 13 and the initial head CT did not demonstrate SAH with a Rotterdam score of 0. There were multiple fractures and soft tissue contusions noted on imaging which required surgical correction and splinting. The patient’s hospital stay was complicated by a large retroperitoneal hematoma requiring blood transfusions and surgical evacuation. 16 days after admission, the patient experienced sudden‐onset right upper extremity paralysis and weakness of the right leg. CT head demonstrated loss of gray‐white differentiation in the left middle cerebral artery (MCA) territory and CT angiography demonstrated 70% stenosis of the left supra‐clinoid internal carotid artery (ICA) and proximal left MCA. Cerebral angiography demonstrated 60% stenosis left supra‐clinoid ICA and 60% stenosis at the origin of the left MCA consistent with PTV. Left MCA stenosis improved to 20% post 10 mg intra‐arterial milrinone in the left ICA (Figure 1). The patient also received verapamil orally. Transcranial doppler demonstrated elevated peak systolic velocities at 298 cm/s in the left MCA and 276 cm/s in the left ICA. Six days later this improved to 150 cm/s in the left MCA and 151 cm/s in the left ICA. The patient continued to be unable to move her right side against gravity with dense expressive aphasia and dysarthria at discharge to inpatient rehabilitation. At follow‐up 4 weeks later, her right hemiparesis had improved significantly to being able to stand with assistance and her expressive aphasia had improved from one word to occasionally forming several word sentences. Conclusions : PTV is a potentially devastating complication of TBI. As our case demonstrates, the presence of mild TBI and absence of SAH may be falsely reassuring. 2 Additionally, our case report demonstrates that intra‐arterial milrinone causes radiographic improvement in PTV. Further studies are needed for the best screening and diagnostic exams for PTV and therapeutic interventions.

Transcranial Doppler Ultrasound Pre and Post Middle Cerebral Artery Stent Placement

This report describes a 42 year old male with a 5 year history of transient ischemic attacks (TIAs), migraines, previous strokes, and symptoms referable to a left middle cerebral artery (MCA) territory event. Computed tomography angiography (CTA) and magnetic resonance angiography (MRA) revealed severe stenoses in the proximal left MCA and proximal left anterior cerebral artery (ACA). Transcranial Doppler ultrasound/Transcranial Doppler imaging (TCD/TCI) and cerebral angiogram confirmed the stenoses with a mean flow velocity (MFV) at the proximal left MCA, with a velocity of 230 cm/s. A Wingspan Stent System stent was placed in the proximal left MCA. Cerebral angiogram and serial TCD examinations performed post stent placement showed a patent left MCA without stenosis and a MFV of 55 cm/s. The left ACA was occluded following proximal left MCA stent placement. This case highlights the usefulness of TCD in the assessment of the MCA and other basal cerebral arteries.

PP04.3 – 2650: Varicella angiopathy: The current challenges of management

Stroke secondary to varicella angiopathy commonly occurs in healthy children presenting with hemiparesis with a history of Varicella Zoster Virus (VZV) infection less than 12 months earlier. It accounts for approximately 31% of all children presenting with arterial ischaemic strokes. With recent advances in intrathecal antibody testing clinicians are faced with novel challenges in the management of these children. We describe a 4-year-old child who presented to the emergency department with right arm and leg weakness, slurred speech, and right-sided facial weakness over the previous few hours. He had three episodes in the previous six months characterised by a sudden drop to the ground, without loss of consciousness or jerking. In thirty minutes he had returned to normal activity. MRI brain confirmed multiple focal areas of infarction in the left cerebral hemisphere. MRA showed significant abnormal narrowing of the terminal left internal carotid and proximal left middle cerebral artery. CSF testing confirmed active VZV infection with intrathecal antibody production. A literature search confirmed that in adults, characteristic ischaemic lesions in the setting of positive CSF markers are considered the consistent criteria for diagnosis of varicella angiopathy with no clear diagnostic guidelines for children. Equally there is no consensus in treatment with authors recommending combination of antiviral and immunosuppressive therapy, others anticoagulant and antiplatelet medication. In this case Infectious Disease and Virology consults were sought and a five-week course of intravenous Acyclovir was commenced with oral aspirin. Repeat CSF testing showed no improvement in VZV IgG levels. Following a 3-month course of oral valciclovir, repeat testing confirmed treatment of VZV infection. MRI and MRA showed persistent arterial narrowing and some resolution in areas of infarction. This case illustrates the challenges faced in diagnosis and treatment for children presenting with stroke suspected secondary to Varicella angiopathy and the benefits of multiprofessional working.

Herpes Simplex Viral Encephalitis Masquerading as a Classic Left MCA Stroke.

Objective. Stroke is a clinical diagnosis, with a history and physical examination significant for acute onset focal neurological symptoms and signs, often occurring in patients with known vascular risk factors and is frequently confirmed radiographically. Case Report. A 79-year-old right-handed woman, with a past medical history of hypertension, hyperlipidemia, and prior transient ischemic attack (TIA), presented with acute onset global aphasia and right hemiparesis, in the absence of fever or prodrome. This was initially diagnosed as a proximal left middle cerebral artery (MCA) stroke. However, CT perfusion failed to show evidence of reduced blood volume, and CT angiogram did not show evidence of a proximal vessel occlusion. Furthermore, MRI brain did not demonstrate any areas of restricted diffusion. EEG demonstrated left temporal periodic lateralized epileptiform discharges (PLEDs). The patient was empirically loaded with a bolus valproic acid and started on acyclovir, both intravenously. CSF examination demonstrated a pleocytosis and PCR confirmed the diagnosis of herpes simplex viral encephalitis (HSVE). Conclusions. HSVE classically presents in a nonspecific fashion with fever, headache, and altered mental status. However, acute focal neurological signs, mimicking stroke, are possible. A high degree of suspicion is required to institute appropriate therapy and decrease morbidity and mortality associated with HSVE.

In Vivo MR Imaging of Intraarterially Delivered Magnetically Labeled Mesenchymal Stem Cells in a Canine Stroke Model

BackgroundThis study aimed to evaluate the feasibility of intraarterial (IA) delivery and in vivo MR imaging of superparamagnetic iron oxide (SPIO)-labeled mesenchymal stem cells (MSCs) in a canine stroke model.MethodologyMSCs harvested from beagles’ bone marrow were labeled with home-synthesized SPIO. Adult beagle dogs (n = 12) were subjected to left proximal middle cerebral artery (MCA) occlusion by autologous thrombus, followed by two-hour left internal carotid artery (ICA) occlusion with 5 French vertebral catheter. One week later, dogs were classified as three groups before transplantation: group A: complete MCA recanalization, group B: incomplete MCA recanalization, group C: no MCA recanalization. 3×106 labeled-MSCs were delivered through left ICA. Series in vivo MRI images were obtained before cell grafting, one and 24 hours after transplantation and weekly thereafter until four weeks. MRI findings were compared with histological studies at the time point of 24 hours and four weeks.Principal FindingsHome-synthesized SPIO was useful to label MSCs without cell viability compromise. MSCs scattered widely in the left cerebral hemisphere in group A, while fewer grafted cells were observed in group B and no cell was detected in group C at one hour after transplantation. A larger infarction on the day of cell transplantation was associated with more grafted cells in the brain. Grafted MSCs could be tracked effectively by MRI within four weeks and were found in peri-infarction area by Prussian blue staining.ConclusionIt is feasible of IA MSCs transplantation in a canine stroke model. Both the ipsilateral MCA condition and infarction volume before transplantation may affect the amount of grafted cells in target brain. In vivo MR imaging is useful for tracking IA delivered MSCs after SPIO labeling.

A novel embolic stroke model resembling lacunar infarction following proximal middle cerebral artery occlusion in beagle dogs

It is estimated that lacunar infarcts account for 25% of all ischemic strokes, but its exact etiology is still on debating. The existing controversies include whether the embolisms can indeed cause lacunar stroke in humans or animal models. We hypothesized that lacunar infarction can be induced by the proximal middle cerebral artery (MCA) segmental occlusion involving the orifices of lenticulostriate arteries in animal models, which have abundant distal cerebral collateral anastomosis. Our work here establishes a proximal MCA occlusion model using thrombi (autologous blood clots about 1.7mm in diameter and 5mm in length) in 8 beagle dogs, evaluates the progression of ischemic lesions at 30min interval within 6h after embolization using the diffusion weighted imaging (DWI), and discusses the potential mechanisms of lacunar infarction. Our results indicate that the left proximal MCAs can be successfully occluded in all dogs using interventional single-thrombus method. The small solitary or multiple ischemic lesions shown in DWI were observed in the deep brain area, with the mean detecting time of 1.21±0.45h using DWI and diameter of 6.62±0.60mm in 6h-DWI after procedure. In conclusion, our method established an ischemic model which can recapitulate the radiologic and histologic changes in lacunar infarcts, suggesting that emboli can cause lacunar infarcts in animal model.

A Palpable Source of Stroke

A 68-year-old patient was admitted with right-sided hemiplegia and dysarthria of sudden onset. His medical history included bipolar disorder, past alcohol and cigarette abuse, and untreated arterial hypertension. Clinical examination revealed a pulsatile mass in the upper epigastric region and diastasis recti, which were congenital, according to the patient. The cardiac rhythm was atrial fibrillation. Chest radiography showed rightward deviation of the heart (Figure 1A). Thoracoabdominal computed tomography disclosed protrusion of the left ventricular apex into the epigastric region, containing a round hypodense mass suggestive of a thrombus (Figure 1B). Cerebral computed tomography showed an occlusive thrombus of the proximal left middle cerebral artery without any early sign of brain ischemia (Figure 2A). Figure 1. A , Chest x-ray showing rightward deviation of the heart. B , Thoracoabdominal computed tomography, sagittal reconstruction, showing protrusion of the left ventricular apex of the heart into the epigastric region (arrow). Figure 2. A , Cerebral computed tomographic arteriography, coronal reconstruction, …

Hemiconvulsion-Hemiplegia-Epilepsy Syndrome Associated With CACNA1A S218L Mutation

Hemiconvulsion-hemiplegia-epilepsy syndrome involves sudden and prolonged unilateral seizures, followed by transient or permanent hemiplegia and epilepsy during infancy or early childhood. Some patients with familial hemiplegic migraine and demonstrating the S218L mutation in CACNA1A experience severe attacks with unilateral cerebral edema after trivial head trauma. We report on a 5-year-old Japanese girl presenting with hemiconvulsion-hemiplegia-epilepsy syndrome after infection with parvovirus B19. Magnetic resonance imaging performed 2 days after admission revealed cerebellar atrophy and marked hyperintensity in the left hemisphere on T(2)-weighted and diffusion-weighted imaging. Magnetic resonance angiography performed 7 days after admission demonstrated obliteration of the left proximal middle cerebral artery in the acute phase. However, this finding was not evident on brain angiography performed 25 hours after magnetic resonance angiography. Genetic analysis of familial hemiplegic migraine revealed a heterozygous S218L mutation in CACNA1A. Taken together, these results suggest that vasospasms of cerebral vascular smooth muscle, with possible cortical spreading depression, may have caused the hemiconvulsions and hemiplegia in the left hemisphere. This case report is the first, to the best of our knowledge, to associate CACNA1A with hemiconvulsion-hemiplegia-epilepsy syndrome and familial hemiplegic migraine, and to suggest that similar pathogenic mechanisms may underlie these two disorders.

Endovascular Coil Embolization of a Ruptured Distal Anterior Choroidal Artery Aneurysm Associated With Ipsilateral Middle Cerebral Artery Occlusion -Case Report-

An 84-year-old woman with a history of hypertension and a brain infarction presented with a rare distal anterior choroidal artery (AChoA) aneurysm not associated with moyamoya disease manifesting as sudden onset of headache caused by intraventricular hemorrhage. Digital subtraction angiography revealed a peripheral aneurysm in the left AChoA located distal to the plexal point and steno-occlusive changes of the proximal left middle cerebral artery (MCA) and the left posterior cerebral artery (PCA). Collateral arterial channels to the left MCA and left PCA territories were observed along the left AChoA. No neuroimaging findings were compatible with moyamoya disease. Since the aneurysm did not shrink at 2 months after the onset, endovascular treatment was indicated. Under local anesthesia, a microcatheter was placed into the AChoA proximal to the aneurysm with the aid of a 0.008-inch microguidewire. After a provocation test, three detachable platinum coils were delivered into the aneurysm and the parent artery. Complete obliteration of the aneurysm was achieved without additional neurological sequelae. Successful treatment of a ruptured distal AChoA aneurysm associated with atherosclerotic changes of the intracranial arteries was achieved using a meticulous endovascular technique.

Ultrasonic Assessment of Cerebral Blood Flow Changes During Ischemia-Reperfusion in 7-Day-Old Rats

A model of ischemic brain injury in 7-day-old rat pups has been developed to study perinatal ischemia. It combines permanent occlusion of the distal left middle cerebral artery (LMCA) and transient occlusion of homolateral common carotid artery (LCCA). At removal of the clip on LCCA, reflow allowed brain reperfusion through cortical anastomoses. In 10 rat pups, we measured blood flow velocities (BFV) in main cerebral arteries with 12-MHz ultrasound imaging. At basal states, peak systolic BFV in proximal LMCA was 16.0 ± 3.0 cm.s –1. Occlusion of LMCA did not yield significant modifications. Occlusion of LCCA involved only a decrease in BFV to 9.5 ± 2.6 cm.s –1 ( p < 0.001). Indeed, LMCA was then supply by the right internal carotid and the vertebral arteries through the circle of Willis. In three rat pups, release of occlusion of LCCA was followed by restoration of BFV in the left internal carotid artery and in LMCA, in seven pups, by a reversed flow in the LICA and lower BFV in LMCA (11.9 ± 2.3, p < 0.05). BFV returned to basal values from h5 to h48 in all animals. In addition, ultrasound imaging is a useful, reproducible, non invasive, easy-to-repeat, method to assess and monitor arterial cerebral blood flow supply in small animals. It helps to characterize changes occurring during cerebral ischemia and reperfusion, particularly the depth of the hypoperfusion, as well as the variability of reflow. In preclinical studies, this method could help to identify what can be assigned to a neuroprotective treatment and what depends on changes in cerebral blood flow supply. (E-mail: philippe.bonnin@lrb.aphp.fr)

Disappearance and reappearance of a cerebral aneurysm: a case report

The false-negative rate of DSA in the setting of a ruptured cerebral aneurysm is approximately 15% (Topcuoglu M, Ogilvy C, Carter B, et al. Subarachnoid hemorrhage without evident cause on initial angiography studies: diagnostic yield of subsequent angiography and other neuroimaging tests. J Neurosurg 2003;98:1235-1240). Detecting these aneurysms is imperative to avoid repeat hemorrhage. Rarely, one is able to document the phenomenon of the disappearance and subsequent reappearance of the ruptured aneurysm. This is a case report of subarachnoid hemorrhage (SAH) in which a cerebral aneurysm of the M1 segment of the left proximal middle cerebral artery was initially detected by CTA at an outside hospital only to evade detection with both CTA and DSA at our institution. Repeat DSA 1 week later revealed the culprit aneurysm, which was then treated endovascularly. Patients with significant SAH and negative DSA findings should be considered for further diagnostic testing including CTA or repeat DSA. The current literature supports the strategy used at our institution of initial CTA and DSA in the setting of SAH, and then subsequent repeat DSA as warranted if the initial studies are nondiagnostic. Timing of repeat examination, as demonstrated in this case, should favor a shorter time course.

Postoperative Intracranial Thrombolysis and Angioplasty

The case study involves a patient presenting middle cerebral artery thrombosis, related to a severe vasospasm following subarachnoid hemorrhage due to aneurysm rupture. The patient was treated initially by surgical clipping of the left middle cerebral artery aneurysm. After surgery, the neurological status of the patient was normal. Six days later, the patient presented right hemiplegia and aphasia that were related to the proximal left middle cerebral artery thrombosis. Despite recent open-skull surgery, in situ thrombolysis using urokinase and antip late let antibodies (abciximab) was performed. The thrombosed artery was reopened and a severe vasospasm was observed. The vasospasm was treated by transluminal angioplasty. No intracranial hemorrhage was noted after thrombolysis and angioplasty, whereas subcutaneous hemorrhage around the scalp incision was observed. The patient recovered from motor and language impairment. The only long-term symptom was a mild dysorthographia. Balance of risk/benefit is discussed for such aggressive thrombolytic therapy. In this particular case, effectiveness and uneventful use of abciximab was demonstrated despite very recent brain surgery that was considered a formal contra-indication for the use of such a powerful thrombolytic drug. Vessel thrombosis is an exceptional complication of cerebral vasospasm. In the early hours, intra-arterial thrombolysis may be considered, but recent intracranial surgery is usually an exclusion criterion to performing thrombolysis. We report the case of a patient who underwent thrombolysis and angioplasty in the postoperative period to treat this complication of vasospasm.

Three-vessel occlusion using a micro-clip for the proximal left middle cerebral artery produces a reliable neocortical infarct in rats

We demonstrate a new three-vessel occlusion model of temporary focal ischemia in Sprague–Dawley rats ( n=13). Under a surgical microscope, bilateral carotid arteries and the left middle cerebral artery (MCA) were occluded for 2 h using a snare for the neck and a micro-clip for the MCA. The reduction of regional cerebral blood flow (rCBF) monitored by laser Doppler flowmetry was 28% on average compared to the preischemic control value (100%) during ischemia. At that level of CBF reduction, there was no thrombus formation in the proximal MCA trunk, and a full recovery of rCBF was confirmed in the ischemic core within 5 min of reflow. Two days later, the cerebral infarct was limited to the neocortex, and the size and variability of the infarct are considered feasible for the assessment of any therapeutic challenge against the ischemic damage due to temporary focal ischemia in this model. Themes: Disorders of the nervous system Topics: Ischemia

Susceptibility to Cerebral Infarction in the Stroke-Prone Spontaneously Hypertensive Rat Is Inherited as a Dominant Trait

Susceptibility to cerebral infarction was compared in stroke-prone spontaneously hypertensive (SHRSP), normotensive Wistar-Kyoto (WKY) rats, and F1 hybrids derived from a SHRSP/WKY cross. The proximal left middle cerebral artery (MCA) was occluded under anesthesia and infarct volume assessed 24 hours later by magnetic resonance imaging and confirmed 5 days later by quantitative histopathology. Total hemispheric infarct volume was expressed as a percentage of the total brain volume. Infarct volumes measured by MRI in adult SHRSP (19.5 +/- 2.0%) and F1 hybrid rats (19.4 +/- 1.9%) were significantly greater than in WKY (11.1 +/- 2.4; CI [6.07, 10.76]) and (5.93, 10.52), respectively, P<.001). Sensitivity to an ischemic insult was unrelated to blood pressure: although systolic blood pressures differed between young versus adult male SHRSP and between female versus male SHRSP and F1 hybrids, infarct volumes were equal. A close correlation was found between infarct volumes measured by MRI and histology (r=.92, P<.0001). Outcome to MCA occlusion (MCAO) measured with MRI provides a reproducible and nonterminal quantitative phenotypic marker of stroke susceptibility in the SHRSP. This is the first study to employ MCAO with MRI to quantify stroke susceptibility in F1 hybrid rats and indicates a dominant mode of inheritance for this phenotype.

Methionine sulfoximine reduces cortical infarct size in rats after middle cerebral artery occlusion.

The methionine analogue methionine sulfoximine was administered to 10 rats 24 hours before occlusion of the proximal left middle cerebral artery. Three days later the rats were decapitated and the brain infarct volumes were compared with those in 10 control rats that received saline before middle cerebral artery occlusion. The mean volume of the infarct in the cerebral cortex was reduced by 33% in the group treated with methionine sulfoximine (p less than 0.01). This protective effect may be mediated by a presynaptic mechanism; methionine sulfoximine profoundly inhibits brain glutamine synthetase, thereby interrupting the astrocyte-neuron glutamate shuttle and impairing neuronal glutamate release. Methionine sulfoximine also increases brain glycogen stores, and this increased energy reserve may benefit penumbral tissue during the peri-infarct period. Further study of the mechanisms by which methionine sulfoximine decreases infarct volume could lead to new therapeutic approaches for stroke.

Effects of middle cerebral artery occlusion on baroreceptor reflex control of heart rate in the rat

Neurons in the insular cortex have recently been shown to innervate medullary autonomic nuclei such as the nucleus tractus solitarii (NTS). The present study examines the effect of lesioning the insular cortex on baroreceptor-heart rate reflex in conscious rats. We did this by occluding the stem of the left proximal middle cerebral artery which causes a lesion of the insular and adjacent lateral frontoparietal cortices. Nine and 10 days after lesioning or sham operation, reflex heart rate responses were recorded following i.v. doses of the pressor agent phenylephrine and the depressor agent sodium nitroprusside. Baroreceptor reflex parameters were determined by computerized sigmoidal curve-fitting. The overall contribution of the sympathetic and the cardiac vagus were assessed by using peripherally acting muscarinic and β-adrenoceptor antagonists, respectively. Lesioned rats were compared to sham-operated rats. Lesioning the insular cortex did not affect mean blood pressure and heart rate. However, the lesion selectively enhanced reflex vagal bradycardia that occurred when mean blood pressure was artificially elevated. A greater vagal bradycardia with no change in the upper plateau indicated that ischemia was acting entirely on the baroreflex-dependent vagal cardiac motoneurons. There was no effect on the sympathetic heart rate range but the normalized gain of the sympathetic component was increased in those lesioned rats. These observations suggest that the unilateral cortical lesion chronically affected the baroreceptor control of heart rate through mechanisms differentially affecting the vagus and the cardiac sympathetic nerves.