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[Lacunar brain infarct in carotid occlusion].

The etiology of lacunar CCT lesions is controversial. We report a patient with recurrent ischemia in the territory of the right internal carotid artery. CCT initially showed a fresh non-lacunar lesion in the area of the basal ganglia and internal capsule. Subsequently, repeat CCT revealed a singular lacunar defect in the internal capsule. The Doppler sonographic investigations showed an internal carotid artery occlusion. This case supports the hypothesis that an embolic or hemodynamic etiology of the lacunae is possible.

Aged↗

Microstructural brain development after perinatal cerebral white matter injury assessed by diffusion tensor magnetic resonance imaging.

OBJECTIVE: Brain injury in premature infants is characterized predominantly by perinatally acquired lesions in the cerebral white matter (WM). The impact of such injury on the subsequent development of cerebral WM is not clear. This study uses diffusion tensor magnetic resonance imaging (MRI) to evaluate the effects of cerebral WM injury on subsequent microstructural brain development in different WM areas of the brain. METHODS: Twenty premature infants (gestational age: 29.1 +/- 1.9 weeks) were studied by conventional MRI within the first 3 weeks of life and again at term, with the addition at the latter time of diffusion tensor MRI. Ten of the preterm infants had cerebral WM injury identified by the early MRI and were matched with 10 premature infants of similar gestational age and neonatal course but with normal neonatal MRI scans. Diffusion tensor MRI at term was acquired in coronal and axial planes and used to determine the apparent diffusion coefficient, a measure of overall restriction to water diffusion, and the relative anisotropy (RA), a measure of preferred directionality of diffusion, in central WM, anterior frontal WM, occipital WM, temporal WM, and the posterior limb of the internal capsule. Diffusion vector maps were generated from the diffusion tensor analysis to define the microstructural architecture of the cerebral WM regions. RESULTS: At term, the diffusion tensor MRI revealed no difference in apparent diffusion coefficient among preterm infants with or without perinatal WM lesions. By contrast, RA, the measure of preferred directionality of diffusion and thereby dependent on development of axonal fibers and oligodendroglia, was 25% lower in central WM, the principal site of the original WM injury. However, RA was unaffected in relatively uninjured WM areas, such as temporal, anterior frontal, and occipital regions. Notably, RA values in the internal capsule, which contains fibers that descend from the injured cerebral WM, were 20% lower in the infants with WM injury versus those without. Diffusion vector maps showed striking alterations in the size, orientation, and organization of fiber tracts in central WM and in those descending to the internal capsule. CONCLUSIONS: Perinatal cerebral WM injury seems to have major deleterious effects on subsequent development of fiber tracts both in the cerebral WM and more distally. The ultimate impact of brain injury in the newborn should be considered as a function not only of tissue destruction, but also of impaired subsequent brain development.

Humans↗

Lesion topography and outcome after thermocapsulotomy or gamma knife capsulotomy for obsessive-compulsive disorder: relevance of the right hemisphere.

OBJECTIVES: Obsessive-compulsive disorder is a common mental disorder, notorious for its chronicity and intractability. Stereotactic lesions within the anterior limb of the internal capsule have been shown to provide symptomatic relief in such refractory cases, but only few systematic evaluations have correlated anatomic lesion location with individual postoperative outcome. PATIENTS AND METHODS: Between 1976 and 1989, extremely disabled and otherwise intractable patients with a chronic deteriorating clinical course of obsessive-compulsive disorder underwent bilateral thermocapsulotomy (n = 22) or radiosurgical gamma knife capsulotomy (n = 13) at the Karolinska Hospital, Stockholm. Clinical morbidity was monitored prospectively pre- and postoperatively by using standardized psychiatric rating scales. In 29 patients (thermocapsulotomy, n = 19; gamma knife capsulotomy, n = 10), both psychiatric and magnetic resonance imaging follow-up data (median, 8.4 yr) were available. RESULTS: A right-sided anatomically defined lesion volume was identified in all successfully treated patients. This common topographic denominator was defined in the approximate middle of the anterior limb of the internal capsule on the plane parallel to the anterior commissure-posterior commissure line at the level of the foramen of Monro and 4 mm above on the plane defined by the internal cerebral vein. This region was unaffected in patients with poor outcomes. On the left side, no particular lesion topography was associated with clinical outcome. Topographic differences of lesion overlap between good and poor outcome groups were significant for the right side (Fisher's exact test, P < 0.005). CONCLUSION: The current anatomic long-term analysis after thermocapsulotomy or gamma knife capsulotomy for obsessive-compulsive disorder reveals common topographic features within the right-sided anterior limb of the internal capsule independent of treatment modality.

Adult↗

[Dysarthria due to small cerebral infarction--the localization of lesion and clinical characteristics].

We compared locations of infarctions and clinical characteristics for patients with dysarthria and those without dysarthria. Subjects were 40 patients with a small infarction in the corona radiata or junctional zone to the capsule and 13 patients with infarctions in the internal capsule. Left corona radiata/junctional zone infarctions were significantly smaller than right sided lesions. Dysarthria was associated more frequently with the corona/junctional lesions on the left side than the right sided lesions. Asymptomatic infarctions on the contralateral side were seen in 41% of the patients with dysarthria. In these cases, dysarthria continued longer and dysphagia occurred more frequently than the cases without right sided lesions. Corona radiata/junctional zone infarctions with dysarthria were located significantly more anteriorly than those without dysarthria. The corona radiata/junctional zone infarctions presenting with dysarthria alone, upper limb dominant hemiparesis, and lower dominant hemiparesis were located in the anterior, middle, and posterior areas, respectively. In conclusion, dysarthria may occur with unilateral small cerebral infarctions, more frequently with left sided lesions than with right sided lesions. It is assumed that the left corona radiata/junctional zone infarction may interrupt simultaneously the corticobulbar pathway and callosal fibers to the right hemisphere which transmit motor information for speech to the right hemisphere. It is also possible that there are individual variations in the proportion of crossed and uncrossed corticobulbar innervation, which may explain dysarthria with unilateral cerebral lesions in some patients. It was suggested that there is an anterior-posterior somatotopy in the corona radiata/junctional zone as well as in the internal capsule.

Cerebral Infarction↗

Ischemia-induced accumulation of extracellular amino acids in cerebral cortex, white matter, and cerebrospinal fluid.

In a global model of brain ischemia, accumulation of amino acids was studied in the extracellular space of the auditory cortex and the internal capsule using microdialysis, and in CSF of halothane anesthetized cats. In both brain regions, blood flow determined by hydrogen clearance decreased below 10 ml/100 g/min after extracranial multiple-vessel occlusion, and extracellular potassium activity (Ke) measured in the dialysate increased significantly. A delayed rise in Ke was observed in CSF. In contrast, ischemic amino acid accumulation differed markedly between the two brain regions investigated. In cortex, transmitter amino acids glutamate, aspartate, and gamma-aminobutyric acid (GABA) rose almost immediately after onset of ischemia, and increased 30-, 25-, and 250-fold, respectively, after 2 h of ischemia. The nontransmitter amino acids taurine, alanine, and serine increased 10-, seven-, and fourfold, respectively, whereas glutamine and essential amino acids (valine, phenylalanine, isoleucine, and leucine) increased only 1.5-fold. In the internal capsule, increases in amino acids, if any, were delayed and much smaller than in cortex. The largest alteration was a fivefold elevation of GABA. In CSF, changes in amino acids were small and comparable to those in the internal capsule. Our results demonstrate that ischemia-induced extracellular amino acid accumulation is a well localized phenomenon restricted to gray matter structures that possess release and reuptake systems for these substances. We assume that amino acids diffuse slowly into adjacent while matter structures, and into CSF.

Amino Acids↗

MRI of hyperacute stroke in the AChA territory.

The purpose of our study was to derive from the anatomical literature an easy-to-use map of the brain areas supplied by the anterior choroidal artery (AChA) and to assess the correspondence between damage within the putative AChA areas and clinical symptoms. A thorough review of the literature led to the recognition of 16 anatomical areas which could be delineated on routine diffusion-weighted MR images. A database of 138 consecutive ischemic stroke patients examined with MRI less than 6 h after symptoms onset was thereafter processed in a retrospective way. Patients presenting with at least one damaged AChA area were selected so as to assess the prevalence of AChA infarction and the clinical correlates of the condition. Fifteen patients (11%) had at least one damaged AChA area. Only two of them had "pure" AChA-restricted infarction. Contralateral hemiparesis and contralateral hemianesthesia were best predicted by lesions within the tail of the caudate nucleus with a sensitivity of 87% and 83%, respectively. Homonymous hemianopsia best correlated with lesions within the posterior limb of the internal capsule and within the retrolenticular part of the internal capsule, with a sensitivity of 100% and a specificity of 70% for both areas. We concluded that the clinical-radiological correlations did not match the neurophysiological standards, thereby highlighting the limitation of this study, which involved a cohort of acute stroke patients recruited from clinical practice and investigated the clinical impact of these brain lesions, even when documented with the most sensitive imaging modality.

Acute Disease↗

Ocular tracking of step-ramp targets by patients with unilateral cerebral lesions.

The relationship of sinusoidal smooth pursuit defects to pursuit defects with step-ramp targets in patients with cerebral lesions is unclear. We examined pursuit and saccades to both step-ramp and sinusoidal targets in 17 patients with unilateral cerebral lesions. Two types of pursuit defects were found. One group of three patients had ipsi-directional sinusoidal pursuit defects from lesions to the posterior internal capsule. Their chief abnormality with step-ramp targets was increased contra-directional pursuit. Their ipsi-directional step-ramp pursuit was often normal and disproportionately better than their ipsi-directional sinusoidal pursuit. Another patient with a parietal lesion had a second type of pursuit defect. He had low-normal sinusoidal pursuit bilaterally, but decreased ipsi- and contra-directional step-ramp pursuit. Also, he had an abnormal contra-directional drift after saccades to stationary targets. Despite these pursuit defects, saccadic accuracy did not show poor compensation for target motion in either patient type. The patient with the parietal lesion also had increased latencies for contralateral saccades. Recovery of pursuit was studied in one patient with an infarct of the posterior internal capsule. Initially he had a contra-directional bias that caused decreased ipsi-directional pursuit, increased contra-directional pursuit, and a contra-directional drift after saccades to stationary targets. Four months later, ipsi-directional pursuit and the post-saccadic drift to stationary targets had recovered, but contra-directional pursuit remained abnormally high. We conclude that lesions of descending pursuit tracts in the internal capsule are characterized by a contra-directional bias which recovers partly through a direction-specific adaptation. Lesions that affect the human homologue of posterior parietal cortex cause asymmetric bi-directional defects in pursuit initiation and increased contralateral saccadic latencies.

Adult↗

Connectional distinction between callosal and subcortically projecting cortical neurons is determined prior to axon extension.

In adult rats, layer 5 cortical neurons send axons through the corpus callosum to contralateral cortex or through the internal capsule to subcortical targets, but individual neurons reportedly do not have both connections. Here we confirm this adult separation and address whether it develops by extension of axon collaterals to both sets of targets with later elimination of one or the other (a phenomenon common in developing cortex) or by initially selective axon outgrowth. Retrograde tracers Fast Blue and Diamidino Yellow were injected in the subcortical path at the pyramidal decussation and in the contralateral cortex, respectively, of adult and newborn rats. In 16 adults, no cortical neurons were double-labeled, indicating that none project to both sites. In 17 neonates, hundreds of thousands of layer 5 neurons were single-labeled in each brain, but only one was double-labeled. In cases in which the injections to one of the two targets was delayed, again, no double-labeled cells were found. These results indicate that the connectional distinction found in adults is not achieved by the elimination of long transient callosal or subcortical collaterals. To determine if shorter transient collaterals are extended by callosal neurons into the internal capsule, i.e., the subcortical pathway, we injected DiI into one cortical hemisphere of aldehyde-fixed Embryonic Day (E)19 and E21 brains. Two types of axons are seen in the white matter of the cortex opposite the injection: those which turn and extend through the callosum and those which branch, sending collaterals to both ipsilateral and contralateral cortex. Rarely were collaterals seen to extend into or toward the internal capsule. [3H]Thymidine birthdating studies show that layer 5 callosal and subcortically projecting neurons are generated at the same stage of corticogenesis. Thus, from early stages of axon extension, callosal and subcortically projecting cells are distinct classes of neurons and, responding differentially to cues present in cortex, initiate growth toward class-specific and nonoverlapping sets of targets. We conclude that the distinction between the two projection classes in inherent to them and is likely to be determined at an early stage of cortical development, prior to neuronal migration from the neuroepithelium.

Animals↗

Correlating magnetic resonance imaging markers of axonal injury and demyelination in motor impairment secondary to stroke and multiple sclerosis.

The primary pathological mechanisms in stroke and multiple sclerosis (MS) are very different but in both diseases, impairment may arise from a final common pathway of axonal damage. We aimed to examine the relationship between motor impairment, magnetisation transfer ratio (MTR) (an index of demyelination), and N-acetyl aspartate (NAA) loss (an index of axonal injury) localised to the descending motor pathways in stroke and MS. Twelve patients between 1 and 10 months after first ischaemic stroke causing a motor deficit and 12 patients with stable MS with asymmetric motor deficit were examined. T(2)-weighted imaging of the brain together with MTR and proton (voxel 1.5x2x2 cm(3)) MRS localised to the posterior limb of the internal capsule were performed and correlated to a composite motor deficit score. MTR and NAA in the internal capsule were reduced in both stroke and MS patients compared to controls. NAA loss correlated with motor deficit score in both stroke and MS (p<0.001 and p = 0.04, respectively). Correlations were seen between MTR and motor deficit (p<0.001) MTR and NAA loss (p <0.001) in stroke patients but not in MS patients. Axonal injury in the descending motor tracts would appear to be an important determinant of motor impairment in both stroke and MS. In stroke, MTR measures of demyelination are closely related to axonal damage and thus also correlate with motor deficit. However in MS, MTR measures of demyelination do not correlate with NAA loss or motor deficit suggesting that demyelination and gliosis may occur independently of axonal damage and are less closely linked with functional impairment.

Adult↗

Dysembryoplastic neuroepithelial tumour and cerebellar atrophy: case report.

Dysembryoplastic neuroepithelial tumours (DNET) are mainly benign cortical lesions. DNET in the caudate nucleus, thalamus, hypothalamus, pons and cerebellar hemispheres has also been reported. We describe a fronto-temporo-parietal DNET extending to the ipsilateral thalamus and internal capsule, associated with cerebellar lobe atrophy. Involvement of the internal capsule and complication of DNET with cerebellar atrophy have not been reported previously. We emphasise the importance of early diagnosis and treatment of this rare condition.

Atrophy↗

Does very preterm birth impair myelination of the central nervous system?

Myelination of the central nervous system (CNS) can be demonstrated with magnetic resonance (MR) imaging. Myelin formation may be reduced in conditions of neonatal "undernutrition". Very preterm infants have a reduced postnatal growth rate when compared with intrauterine fetuses of the same gestational age. Using MR imaging, we studied qualitative myelination patterns in healthy preterm infants of less than 30 weeks gestation with an optimal nutritional intake and in term infants at 44 weeks postmenstrual age (PMA). At that age, preterm infants had a significantly lower mean body weight than term infants, but mean head circumference did not differ significantly. All preterm and term infants had reached myelination stage M3 (myelin in brainstem, internal capsule, and corona radiata) and M4 (myelin in brainstem, internal capsule, corona radiata, and centrum semiovale). There was no significant difference in myelination stage between the preterm and term infants. We conclude that adequate nutrition in the neonatal period leads to qualitatively adequate myelination of the CNS in very preterm infants.

Central Nervous System↗

The nigrostriatal nervous pathways in the brain of the cat. An autoradiographic study.

By comparing the findings obtained in these series of cats with injections of 3H-leucine involving different areas of the SN and adjacent neurons of the VTA, some conclusions may be drawn concerning the origins, courses, and terminations of the nigrostriatal fibers. Three main bundles of nigrostriatal fibers originating from different groups of neurons of the SN may be identified. The main cluster of neurons of the compacta type, corresponding to the more abundant and larger neurons of this group in the caudal part of the SN and above (pars dorsalis of the SN), gives rise to fibers that leave the latter structure through its dorsomedial lip. They course successively in the VTA and in the area of Tsai and proceed rostralward through the lateral hypothalamus, subthalamus, and the internal capsule. At the level of the anterior limb of the internal capsule, they undergo an important arborization before ending in the putamen and caudate nucleus. Fibers from the main cluster of compacta neurons terminate more dorsally and those from the dorsal part of the SN end more ventrally in the neostriatum. These findings generally agree with those of VanderMaelen et al. (12) and Szabo (9), who applied the HRP technique, and Usunoff et al. (11), who used a selective silver impregnation method in cat brains. In the caudate nucleus, endings from the compacta type neurons are more abundant in certain areas, forming islands of dense silver grains. These areas of dense endings appear to correspond to the areas of greater cellular density of the striatum as more easily recognizable in the caudate nucleus of the newborn cat (Fig. 9).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[Lingual motility in unilateral hemispheric vascular complications. Study of the cortico-hypoglossal afferences].

Lingual motricity was prospectively studied in 32 consecutive stroke patients with hemiparesis or hemiplegia involving the face. We excluded patients with vertebrobasilar infarcts, controlateral stroke, arteriovenous malformations, internal carotid artery dissection, severe aphasia or severe bucco-lingual apraxia. The study population consisted of 18 males and 14 females with a mean age of 64.2 years. Seventeen patients had a lesion located in the right hemisphere and 15 in the left one. The lesion was of ischemic origin in 19 patients and hemorrhagic in 13. Lingual motricity was studied at rest and at protraction. We recorded whether the following abnormalities were present: lingual deviation, limitation of protraction or lateral movements, atrophy, hypotonia and fasciculations. Sixteen patients had a deviation of the tongue at protraction. The other abnormalities were deviation of the tongue at rest, limitation of lateral movements at protraction, unilateral lingual hypotonia and limited protrusion. Of 16 patients with deviation of the tongue at protraction, 10 had no deviation at rest. Of the 6 remainders, 2 had deviation of the tongue towards the opposite side, at rest, and 4 towards the same side. Most patients with deviation of the tongue at protraction, had a lesion of the posterior limb of the internal capsule and of the posterior part of the lenticular nucleus. Most patients without lingual deviation, had a lesion of the capsule-lenticular region and of the superior portion of the internal capsule, just under the corona radiata.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Selective alterations of white matter associated with visuospatial and sensorimotor dysfunction in turner syndrome.

Turner syndrome (TS) is a neurogenetic disorder characterized by impaired spatial, numerical, and motor functioning but relatively spared verbal ability. Results from previous neuroimaging studies suggest that gray matter alterations in parietal and frontal regions may contribute to atypical visuospatial and executive functioning in TS. Recent findings in TS also indicate variations in the shape of parietal gyri and white matter microstructural anomalies of the temporal lobe. Diffusion tensor imaging and structural imaging methods were used to determine whether 10 females with TS and 10 age- and gender-matched control subjects exhibited differences in fractional anisotropy, white matter density, and local brain shape. Relative to controls, females with TS had lower fractional anisotropy (FA) values in the deep white matter of the left parietal-occipital region extending anteriorly along the superior longitudinal fasciculus into the deep white matter of the frontal lobe. In addition, decreased FA values were located bilaterally in the internal capsule extending into the globus pallidus and in the right prefrontal region. Voxel-based morphometry (VBM) analysis showed corresponding white matter density differences in the internal capsules and left centrum semiovale. Tensor-based morphometry analysis indicated that the FA and VBM results were not attributable to differences in the local shape of brain structures. Compared with controls, females with TS had increases in FA values and white matter density in language-related areas of the inferior parietal and temporal lobes. These complementary analyses provide evidence for alterations in white matter pathways that subserve affected and preserved cognitive functions in TS.

Adolescent↗

Development of the amygdalohypothalamic projection in the mouse embryonic forebrain.

The amygdalohypothalamic projection, a major component of the stria terminalis, is involved in the conduction of emotional and olfactory information integrated in the amygdala to the hypothalamus to elicit emotional reactions. Despite the extensive studies on functional aspects of the amygdaloid complex, developmental mechanisms of the amygdala and related structures are still poorly understood. To investigate the development of the amygdalohypothalamic projection in the mouse embryonic brain, carbocyanine dye was applied to the amygdala to label the growing axons anterogradely and to the hypothalamus to label the amygdaloid neurons retrogradely. The initial outgrowth of the stria terminalis was found to be as early as E11.5. The pathway crossed in a saddle over the internal capsule, another prominent connection in the developing forebrain of the mammalian embryo. Bipolar immature neurons were distributed along the stria terminalis at the telencephalo-diencephalic boundary, and the internal capsule was also surrounded by these cells. These cells expressed immunoreactivities to calretinin and the lot-1 antigen which has been shown to be involved in guidance of the developing lateral olfactory tract. Ultrastructural analysis revealed an adherens-like junction between the stria terminalis and the apposed cells, implying contact-mediated guidance. These results suggest that, in the development of the stria terminalis, the axonal outgrowth is guided by a mechanism similar to that of the developing lateral olfactory tract, a major amygdalopetal connection.

Adherens Junctions↗

Light microscopic analysis of Golgi-impregnated rat subthalamic neurons.

The neuronal morphology of the rat subthalamic nucleus (STH) was studied using Golgi techniques and Nissl stain. The results show that the somatic shapes of STH neurons vary from fusiform to oval or polygonal. Somatic cross-sectional areas vary between 140 microns2 and 440 microns2. Some of the cells have a few somatic spines. Two to six primary dendrites gave rise to tapering daughter dendrites which extend up to 500 microns. These dendrites are sparsely covered with spines. Some distal dendrites and primary dendrites of the STH also bear filiform appendages. Neurons located in the deep portion of the STH have oval dendritic fields whose long axis is parallel to the long axis of the nucleus in frontal or sagittal planes. Some of these neurons have one or two dendrites which cross the borders of the STH into the zona incerta, the lateral hypothalamus, or the cerebral peduncle. Generally, neurons located at the borders of the STH have their dendritic fields extending parallel to the borders and are confined to the nucleus. However, some neurons adjacent to the ventrolateral border of the nucleus have some dendrites extending into the cerebral peduncle. Quantitative analysis of the STH neurons showed a unimodal distribution of somatic sizes as well as the number of primary dendrites. No neurons with obvious Golgi type II characteristics were found. Two types of afferent fibers were observed entering the STH. One type consists of axon collaterals arising from the cerebral peduncle ventrolaterally, or the internal capsule rostrally, while the other enters the nucleus after crossing the internal capsule rostrally. These results suggest that the rat STH is an open nucleus in contrast to other species such as man, monkey, and cat, where it is closed, and that the rat STH may contain only one type of neuron.

Animals↗

MRI: early onset of changes in Wallerian degeneration.

T2-weighted spin echo scans were performed on a neonate and two adults aged 42 and 60 years within 2 weeks of the onset of infarction in the frontoparietal region of the brain. Areas of increased signal intensity were observed in the anterior and posterior limbs of the internal capsule in the infant and in the posterior limbs of the internal capsules in the adults. Although these signal changes were typical of the chronic phase of Wallerian degeneration, their onset was much earlier than the 10-14 weeks previously described for this stage in adults. The low level of myelination of white matter tracts at birth, and the relatively sparse myelination of the parietopontine tract may account for the rapid onset of changes in these patients which more closely follows the time course described pathologically for Wallerian degeneration in unmyelinated fibres.

Adult↗

Imaging the pyramidal tract in patients with brain tumors.

The clinical usefulness of diffusion-weighted magnetic resonance imaging (DWI) of the pyramidal tract was evaluated in patients with brain tumors. Five normal volunteers and seven patients with glioma (n = 4) or meningioma (n = 3) near the pyramidal tract underwent coronal echo planar DWI. Greyscale DWIs in each of the three orthogonal diffusion gradients were transformed into graduations, color-coded as red, green or blue, respectively, and then composited to form a combined color image. The entire pyramidal tract was visualized on a single fiber mapping image by combining the upper half of the image slice including the primary motor cortex, the corona radiata and the internal capsule with the lower half of the image slice including the internal capsule, the cerebral peduncle and the ventral brain stem. Fiber mapping images demonstrated the pyramidal tract as a distinct band indicating nerve fiber integrity in all volunteers. The entire pyramidal tract from the primary motor subcortex to the ventral brain stem could be traced. Fiber mapping images showed the ipsilateral pyramidal tract as either discontinuous due to impaired anisotropy or compressed due to mass effect in patients with brain tumors. These findings corresponded well with the pre- and postoperative motor functions. Fiber mapping images are useful for evaluating the white matter neuronal tracts and can provide indications for determining surgical strategy.

Adult↗