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A rare case of metastasis to the spinal subarachnoid space from a non-neuraxial primary tumor is presented. Dissemination was shown by computerized tomography to be via the cerebrospinal fluid from secondary deposits in the central nervous system and meninges. This route would seem to be the most common mode of spread to the spinal subarachnoid space.
Benign, epithelial-lined cysts of the neuraxis may be asymptomatic or may behave as space-occupying lesions. Presentation of three such cysts, including an intramedullary epidermoid cyst, a lumbosacral subcutaneous enteric cyst that has an epithelium resembling ependyma, and a hypophyseal duct cyst, illustrates typical problems encountered. Review of their histogenesis and possible embryogenesis indicates that intracranial ependymal cysts and cysts of the sella turcica are not normally associated with other anomalies and frequently occur after middle age, whereas dermal and enteric cysts occur within the first two decades and are commonly associated with vertebral anomalies and other dysraphic syndromes. Enteric cysts may have a variable histologic appearance, including one resembling ependymal cysts. Recognition of the latter is important because of a possible associated dysraphic syndrome and the presence of an extraneuraxial component with the former but not the latter.
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BACKGROUND: Regional anesthesia (RA) is a major component of multimodal perioperative analgesia in children. Despite proven benefits, pediatric RA practice shows marked inter-institutional and international variability, with global practice patterns remaining largely underreported. This study aimed to characterize current RA practices in a pediatric anesthesia department of a French tertiary university hospital. METHODS: This retrospective observational study of prospectively collected data over one year included all children aged 0-18 years receiving at least one RA procedure. The data analyzed comprised demographics, surgical characteristics, RA techniques, guidance methods, and pharmacologic agents. Each RA procedure was considered an independent event, and patients were stratified into five age groups. RESULTS: Over the study period, 907 patients (6.0 [1.0; 12.0] years) underwent 1073 RA procedures: 894 peripheral blocks (83%) and 179 neuraxial blocks (17%). Peripheral blocks predominated in children >6 months (90%), while 59% of neuraxial RA were in infants <6 months. RA was conducted under general anesthesia in 90% of cases; awake spinal anesthesia in small infants comprised most neuraxial procedures. Ultrasound guidance was used in 98% of peripheral blocks, and pre-puncture scanning preceded 22% of neuraxial procedures. Clonidine was used as an adjuvant in >60% of cases. CONCLUSIONS: This single-center cohort reports one year of pediatric RA practice, characterized by high RA implementation rates. While ultrasound guidance was standard for peripheral blocks, pre-puncture scanning remains infrequently used for neuraxial techniques, highlighting a potential margin for improvement based on current practice. Results highlight selective neuraxial strategies in vulnerable infants and routine adjuvant use to optimize postoperative analgesia. Findings confirm RA feasibility in daily pediatric anesthesia and support multicenter studies evaluating inter-institutional variability and outcomes impact.
PURPOSE OF THE REVIEW: Local anesthetics remain vital to modern medicine, yet their narrow therapeutic window continues to result in complications. This review synthesizes recent literature to define the current landscape of local anesthetic-associated adverse events. RECENT FINDINGS: Perioperative mortality attributable to local anesthetics persists despite sustained safety initiatives and professional society recommendations. Pharmacovigilance and case data identify lidocaine (oropharyngeal, topical, and via local infiltration) as the predominant contributor to adverse outcomes, including death. Local anesthetic systemic toxicity remains an issue, with a recent shift in epidemiology: an increasing proportion of toxic events originates from surgeon- and proceduralist-administered analgesia. Anesthesiologist-controlled methods also cause toxicity via catheter-based delivery and nerve blocks in highly vascular regions. Localized toxicity in the form of high neuraxial contributes to morbidity, with recent reviews reinforcing known risk factors; whereas localized neurotoxicity appears less troublesome when managed appropriately. SUMMARY: The cumulative evidence identifies shifts in the patterns of systemic and localized toxicities. Bupivacaine-based peripheral nerve blocks no longer represent the principal cause of complications because of the advent of ultrasound guidance and lipid emulsion therapy. In contrast, high neuraxial techniques persist as a cause of morbidity, accompanied by intravenous/oropharyngeal lidocaine, proceduralist-administered local infiltration analgesia, and catheter-based delivery.
Food-deprived neonatal rats actively ingest milk that is infused into their mouths through intraoral cannulas. This ingestion is accompanied by behavioral activation. The involvement of various brain regions in ingestion and activation was examined by making transections along the neuraxis from the olfactory bulbs to the anterior pons in 2-day-old rats. Following a 24-hr deprivation period, a series of oral milk infusions was given, and milk intake and activity were measured. Intake was severely reduced only in animals with diencephalic transections. Cuts in front of or behind the diencephalon resulted in normal or slightly decreased intake. In contrast, activity tended to decline as the level of the transection became more caudal. Thus ingestion and its accompanying behavioral activation could be separated neuroanatomically. These results suggest that two brain mechanisms are involved in the ingestive response of the infant rat, one in the diencephalon and another caudal to the mesencephalon. However, behavioral activation appears less discretely organized, involving most of the neuraxis.
1. The origin of the lumbar sympathetic inhibitory outflow to the large intestine was studied by recording simultaneously changes in colonic motility and efferent firing in the lumbar colonic nerves (l.c.n.) following lesions at various levels of the neuraxis. 2. Multiunit recordings from the l.c.n. usually consisted of irregular grouped discharges which were unrelated to spontaneous colonic contractions or to respiratory or cardiac cycles. The firing was depressed by the administration of ganglionic blocking agents or by decentralization of the inferior mesenteric ganglion, indicating that it was post-ganglionic and primarily central in origin. 3. In the majority of experiments colonic motility and l.c.n. firing were not altered by transection of the cervical (C2-C3) or thoracic (T10-T13) spinal cord. However, in these acute spinal animals destruction of the lumbar ventral roots or the lumbar spinal cord markedly enhanced colonic motility and depressed l.c.n. firing. These findings indicate supraspinal mechanisms are not essential for the generation of the lumbar inhibitory outflow to the colon. 4. Transection of the l.c.n. enhanced colonic motility in animals with an intact neuraxis, in acute spinal animals and in animals where the thoracolumbar sympathetic outflow was blocked. It is concluded that peripheral ganglionic as well as spinal pathways can sustain an inhibitory input to the colon. 5. L.c.n. firing was enchanced by stretching or pinching the proximal colon or small intestine or by electrical stimulation of intestinal afferent fibres (Adelta and C fibres) in the l.c.m. and mesenteric branches of the splanchnic nerves. The reflexes occurred via spinal pathways and were blocked by transection of the lumbar dorsal roots. Spontaneous firing in the l.c.n. was also generated by isolated segments of the lumbar spinal cord; however, this firing occurred independently of traditional reflex pathways since it was uanffected by transection of the lumbar dorsal roots. It is concluded that the spontaneous firing must be generated via ventral root afferent pathways or via endogenous oscillator circuits in the lumbar spinal cord.
Metastatic spread of medulloblastoma along the neuraxis by leptomeningeal seeding through the cerebrospinal fluid pathways is well known. The occurrence of extracranial metastases outside the neuraxis has been well established, but the occurrence of intramedullary spinal cord metastases not related to surface seeding is rare. A histologically documented case of the latter type is described.
The anatomy, physiology, and pharmacology of an intrinsic neural network that monitors and modulates the activity of pain-transmitting neurons is reviewed. This system can be activated by opiate administration or by electrical stimulation of discrete brainstem sites. Evidence is presented that its pain-suppressing action is mediated in part by endogenous opiatelike compounds (endorphins). This pain suppression system is organized at three levels of the neuraxis: midbrain, medulla, and spinal cord. Activation of neurons in the midbrain periaqueductal gray matter (by electrical stimulation, opiates, and possibly psychological factors) excites neurons of the rostral medulla, some of which contain serotonin. The medullary neurons, in turn, project to and specifically inhibit the firing of trigeminal and spinal pain-transmission neurons. As part of a negative feedback loop, the output of the pain transmission neurons, i.e., pain itself, is an important factor in activating the pain-suppression system. A neural model which incorporates the experimental findings is proposed, and the clinical implications of the model are discussed.
Myelin carbonic anhydrase (CA) was studied with respect to its development in various brain regions and light and heavy myelin (LM and HM). The data indicate that the specific activity of myelin CA has a clear neuraxial distribution, increasing rostrally. The absolute activities and relative distribution are invariant with age; this suggests the CA activity in myelin is independent of stage and degree of myelination. The studies on HM and LM illustrate that HM, like total myelin, has a constant CA activity during development. In contrast, LM although equal to HM at 14 days, progressively decays to an adult level which is one-fourth that of HM. The distribution of CA in myelin was further investigated by comparing the activity in myelin with that present in the SN4 fraction. The activity in this latter fraction, which is derived from heavy myelin, was found to be 2.2 times higher than that in the myelin fraction. Thus, in the adult there exists an almost ten-fold range of activities among the various myelin fractions, SN4 greater than HM greater than LM. This may indicate a segregation of activity towards the outer lamellae. This segregation may have physiological importance in that it is this region of the sheath which should be integrally involved in control of myelin edema. Evidence indicates that there is an interaction of chloride with the enzyme, and maybe the primary ion moved by CA in order to initiate an osmotic flux out of the sheath. The interaction of chloride with the enzyme is dependent on the CA complex with the membrane in that solubilization and partial (60-fold) purification results in a preparation which is refractory to anions.
6 autopsy cases of primary leptomeningeal sarcomatosis are presented as a distinct nosological entity with a variable clinical picture and morphology in 5 males and 1 female. The clinical course from onset of symptoms till death ran for only a few weeks in most cases. 2 infants showed brain tumor symptoms and signs. 2 patients of advanced age presented a polyradiculoneuritic syndrome and 2 young adults had spinal cord compression symptoms and a mixed clinical form. In almost all cases, clinical symptoms and signs were for most of the course confined to one part of the neuraxis. The CSF was distinctly abnormal in all cases, showing elevated protein, depressed glucose and pleocytosis of variable extent. CSF sediment was investigated in 3 cases in all of which malignant tumor cells were found so a diagnosis of malignant meningeal tumor was made during life. Electron microscopy of CSF cells in 1 case confirmed the primitive character of the tumor cells. Complete autopsies revealed absence of any neoplasm outside of the CNS. Gross meningeal involvement was visible in all cases. Histologically, 3 tumor types were distinguished: polymorphic cell sarcoma, an undifferentiated form, and fibrosarcomatosis. Clinical data are analyzed in order to distinguish the condition from other neoplasms or infectious, especially tuberculous meningeal infiltrations. CSF cytology studies are considered the most useful step in clinical diagnosis. Neuropathological features are reviewed with stress on differentiation from malignant lymphomas of the CNS, diffusely spreading medulloblastoma, meningeal melanoblastosis and gliomatosis. The origin of meningeal sarcomatosis cells is briefly discussed. The use of the term "meningeal meningiomatosis" for this condition is deprecated.
Subpial and subependymal gliosis with abundant Rosenthal fiber (RF) formation are described in two patients. In one, the process appeared as a narrow band over the entire neuraxis and was not accompanied by neurologic manifestations. In the other, the changes were mostly restricted to the lower medulla and upper cervical cord and displayed invasive features. The glial proliferation with RF in the second patient was associated with an inflammatory component, dense collagen deposition, perivascular Schwannosis and demyelination. Involvement of some of the medullary nuclei and their tracts may explain the patient's vague bulbar symptomatology. The underlying cause which led to astrocytic proliferation with excessive RF in these two patients remains elusive. Possible factors contributing to this phenomenon are discussed in the context of Alexander's disease.
The authors present a case of primary carcinoma of the choroid plexus in a 26-years-old female, localized in the left lateral ventricle. Four years after total removal plus local radiotherapy, the patient presented with an intraparenchymatous metastasis in the right cerebellar hemisphere and intraspinal metastatic seeding. With this kind of malignant growth, a therapeutic approach consisting of radical removal of the tumour plus radiotherapy to the whole neuraxis is proposed.
The projections of serotonin-containing neurons of the midbrain raphe nuclei (nucleus raphe dorsalis, nucleus centralis superior) are studied by analysis of axonal transport of labeled amino acids. These results are correlated with regional alterations of serotonin content following midbrain raphe lesions which produce significant serotonin depletion in nearly all regions of the central nervous system. Twenty-four hours following injection of 100 muCi [3H]proline, raphe neurons have taken up labeled material and transported it, presumably as protein, to telencephalon, diencephalon, brain stem, the cerebellum and the spinal cord. This transport appears to take place predominantly in serotonin neurons. After injection of 100 muCi [3H]5-HTP into nucleus raphe dorsalis or nucleus centralis superior, the pattern of regional distribution of transported material is very similar to that obtained with tritiated proline. Selective lesions of serotonin terminals with 5.6-DHT result in greatly diminished axonal transport of proteins to all telencephalic, diencephalic and mesencephalic areas as well as to cerebellum, pons-medulla and spinal cord. Unilateral destruction of the medial forebrain bundle results in significant reduction in axonal transport of labeled material to ipsilateral telencehalon and thalamus. These results provide further support for the view that serotonin neurons of the midbrain raphe nuclei project widely throughout the neuraxis to telencephalon, diencephalon, brain stem, cerebellum and spinal cord.
Slices of frog cerebrum, optic tectum, medulla and spinal cord rapidly accumulate [3H]GABA and [3H]glycine from the surrounding medium so that after 10 min tissue:medium ratios as high as 113 for GABA (optic tectum) and 18.5 for glycine (medulla) may be achieved. Kinetic analysis revealed two distinct saturable uptake systems for each amino acid in the 4 CNS areas. The high affinity systems (apparent Km: 9-22 muM for GABA; 5-35 muM for glycine) required sodium ions in the medium and were relatively substrate specific. Significant release of [3H]GABA and [3H]glycine, but not of L-[3H]leucine, was evoked by exposure to medium containing potassium ions in a concentration of 40 mM. The process of release was calcium-dependent. The importance of these results with regard to the roles of GABA and glycine as neurotransmitters in both spinal and supraspinal levels of the amphibian neuraxis is discussed.