Pulsed Electromagnetic Field (PEMF) Mitigates High Intracranial Pressure (ICP) Induced Microvascular Shunting (MVS) in Rats.

OBJECTIVE: High-frequency pulsed electromagnetic field (PEMF) stimulation is an emerging noninvasive therapy that we have shown increases cerebral blood flow (CBF) and tissue oxygenation in the healthy rat brain. In this work, we tested the effect of PEMF on the brain at high intracranial pressure (ICP). We previously showed that high ICP in rats caused a transition from capillary (CAP) to non-nutritive microvascular shunt (MVS) flow, tissue hypoxia and increased blood brain barrier (BBB) permeability. METHODS: Using in vivo two-photon laser scanning microscopy (2PLSM) over the rat parietal cortex, and studied the effects of PEMF on microvascular blood flow velocity, tissue oxygenation (NADH autofluorescence), BBB permeability and neuronal necrosis during 4 h of elevated ICP to 30 mmHg. RESULTS: PEMF significantly dilated arterioles, increased capillary blood flow velocity and reduced MVS/capillary ratio compared to sham-treated animals. These effects led to a significant decrease in tissue hypoxia, BBB degradation and neuronal necrosis. CONCLUSIONS: PEMF attenuates high ICP-induced pathological microcirculatory changes, tissue hypoxia, BBB degradation and neuronal necrosis.

Characterization of Retinal Ganglion Cell and Optic Nerve Phenotypes Caused by Sustained Intracranial Pressure Elevation in Mice.

Elevated intracranial pressure (ICP) can result in multiple neurologic sequelae including vision loss. Inducible models of ICP elevation are lacking in model organisms, which limits our understanding of the mechanism by which increased ICP impacts the visual system. We adapted a mouse model for the sustained elevation of ICP and tested the hypothesis that elevated ICP impacts the optic nerve and retinal ganglion cells (RGCs). ICP was elevated and maintained for 2 weeks, and resulted in multiple anatomic changes that are consistent with human disease including papilledema, loss of physiologic cupping, and engorgement of the optic nerve head. Elevated ICP caused a loss of RGC somas in the retina and RGC axons within the optic nerve, as well as a reduction in both RGC electrical function and contrast sensitivity. Elevated ICP also caused increased hypoxia-inducible factor (HIF)-1 alpha expression in the ganglion cell layer. These experiments confirm that sustained ICP elevation can be achieved in mice and causes phenotypes that preferentially impact RGCs and are similar to those seen in human disease. With this model, it is possible to model human diseases of elevated ICP such as Idiopathic Intracranial Hypertension and Spaceflight Associated Neuro-ocular Syndrome.

The lucid interval associated with epidural bleeding: evolving understanding.

The aim of this paper was to elucidate the evolution of our understanding of the term "lucid interval." A number of texts were reviewed to assess their suitability for analysis. The primary requirement was that the text contain detailed descriptions of a series of patients. Details of the clinical course, the findings and timing of surgery, and, when relevant, the time of death and postmortem findings were required. Books written by Henri-François Le Dran, Percival Pott, and James Hill fulfilled these criteria. Surgical findings included the presence and type of fractures, changes in the bone, separation of periosteum, malodorous or purulent material, tense brain, and hematoma. Postmortem findings supplemented and/or complemented the surgical findings. The courses of the patients were then tabulated, and the correlation between different clinical and operative findings was thereby determined. Our understanding of a lucid interval began in the early 18th century with the work of Henri-François Le Dran and Percival Pott in London. They did not, however, demonstrate an interval without symptoms between trauma and deterioration in patients with epidural hematomas (EDHs). The interval they described was longer than usually expected with EDHs and occurred exclusively in patients who had a posttraumatic infection. In 1751, James Hill, from Dumfries, Scotland, described the first hematoma-related lucid interval in a patient with a subdural hematoma. The first case of a lucid interval associated with an EDH was described by John Abernethy. In the 19th century, Jonathan Hutchinson and Walter Jacobson described the interval as it is known today, in cases of EDH. The most recent work on the topic came from studies in Cincinnati and Oslo, where it was demonstrated that bleeding can separate dura mater and that hemorrhage into the epidural space can be shunted out via the veins. This shunting could delay the accumulation of a hematoma and thus the rise in intracranial pressure, which in turn would delay the development of symptoms. The lucid interval as previously conceived was not properly understood by the French school or by Percival Pott and Benjamin Bell, who all described a symptom-free period prior to the development of infection. The first to have a proper understanding of the interval in relation to an EDH was John Abernethy. The modern description and definition of the lucid interval was the work of Hutchinson and Jacobson in the latter half of the 19th century. Understanding of the pathophysiology of the lucid interval has been advanced by the work of Ford and McLaurin in Cincinnati and a group in Oslo, with the demonstration of what it takes to loosen dura and how an arteriovenous shunt slows down for a while the accumulation of an EDH.

Symptomatic intracranial hypertension and prolonged hypocalcemia following treatment of Paget's disease of the skull with zoledronic acid.

Skull involvement in Paget's disease of bone can lead to neurological symptoms, prompting treatment. Intravenous zoledronic acid (ZA) has emerged as an effective and safe treatment option for patients with Paget's, leading to sustained remission and improved quality of life. A previously untreated 61-year-old female presented with 2-year history of facial asymmetry with progressive hearing impairment. Serum calcium levels were normal with upper normal levels of PTH and low 25OHD levels. Serum alkaline phosphatase was markedly increased and bone scan showed extensive pagetic involvement of the skull. Head CT and MRI revealed hydrocephalus with cerebellar tonsillar herniation, platybasia and basilar invagination. In the absence of clinical signs or symptoms of intracranial hypertension, she was treated with intravenous ZA after 15-day supplementation with calcium and vitamin D. Twelve hours after the infusion, the patient became confused, agitated and disoriented and developed urinary incontinence; cortical sulci became effaced on CT indicating increased intracranial pressure. Over the following days, she developed frank hypocalcemia requiring intravenous calcium infusion and calcitriol. Neurological status returned to normal within 24 h of onset, except for urinary incontinence. Nine months later she remained incontinent and still required calcitriol to maintain normocalcemia. Zoledronic acid is a first-line option for the treatment of Paget's disease, yet there can be complications in particular clinical scenarios such as pagetic hydrocephalus, as seen in this case. Plentiful supplementation of calcium and vitamin D before bisphosphonate therapy is paramount in order to minimize the risk of prolonged post-treatment hypocalcemia.

Xerophthalmia and intracranial hypertension in an autistic child with vitamin A deficiency.

The authors present a 10-year-old boy with autism and idiopathic intracranial hypertension referred for evaluation of dry eyes. When questioned, the patient's parents reported that he had a restricted diet. Laboratory testing revealed hypovitaminosis A. The symptoms and signs of xerophthalmia rapidly resolved with oral and topical vitamin A supplementation.

Effect of pedal pump and thoracic pump techniques on intracranial pressure in patients with traumatic brain injuries.

CONTEXT: Although osteopathic manipulative treatment (OMT) is used to manage myriad conditions, there has been some hesitation regarding the safety of applying OMT to patients with intracranial injuries or elevated intracranial pressure (ICP). OBJECTIVE: To assess the safety of two OMT techniques--pedal pump and thoracic pump--on ICP and cerebral perfusion pressure (CPP) in patients with traumatic brain injuries (Glasgow Coma Scale score < or =8). METHODS: We prospectively enrolled consecutive patients admitted to the intensive care unit (ICU) for traumatic brain injury. Patients between the ages of 18 and 75 years and with abnormal CT scans were included in the present study. Patients with baseline ICP values of 20 mm Hg or lower were assigned to group 1, and those with ICP levels greater than 20 mm Hg, group 2. Patients underwent continuous ICP and CPP monitoring, with ICP measured using a ventricular catheter and fiber optic device. Values of ICP and CPP were recorded at baseline, during application of the OMT techniques, and 5 minutes after the two OMT techniques were completed. Patients received up to three treatment cycles. Ventricular drains remained open (stopcock open) during OMT, allowing continued cerebral spinal fluid drainage, except for brief periodic closures (stopcock closed) every minute to register accurate ICP values. Statistical analysis was performed using a dependent t test with repeated measures. RESULTS: Twenty-four comatose patients, aged 18 to 69 years, received a total of 50 sessions of pedal pump and thoracic pump techniques. In group 1 patients, a slight decrease in ICP values (mean, -0.586 mm Hg) and an increase in CPP values (mean, 1.1613 mm Hg) was noted post-OMT. Patients in group 2 also had decreased mean ICP values (-1.20 mm Hg) and increased mean CPP values (2.2105 mm Hg). Changes were not statistically significant in either group. CONCLUSION: According to the present limited study, pedal pump and thoracic pump techniques may be used safely in patients with severe brain injuries.

Factors affecting the development of hypothalamus and pituitary lesions in fatal closed head injury: a prospective study.

OBJECTIVES: To determine the factors affecting the development of pituitary and hypothalamic lesions after fatal closed head injury. MATERIALS: Thirty-four patients with severe closed head injury succumbing to the effects of brain trauma before or during admission, whether managed conservatively or surgically, formed the study group. Clinical parameters, injury to death interval, radiologic data, and management details were taken into consideration. Autopsy was performed within 48 hours of death; hypothalamus and pituitary were carefully removed and evaluated for the presence of lesions on hematoxylin and eosin and immunohistochemical staining. RESULTS: Patients were categorized into early death group (n = 11, those succumbing before/on admission) and late death group (n = 23, those succumbing after admission). Histopathologic evaluation of pituitary revealed capsular hemorrhages in 50%, posterior pituitary hemorrhage in 25%, anterior pituitary infarct in 21.8%, and anterior pituitary hemorrhage in 6.2% patients. Hypothalamic hemorrhage was observed in 65.2% patients and infarcts in 17.3%. Lesions in hypothalamus and pituitary were significantly related to the presence of ventricular compression on computed tomography scan and survival of >24 hours after injury (p < 0.05). Capsular hemorrhage, anterior pituitary hemorrhage, and posterior pituitary hemorrhage were present in 40%, 10%, and 30% of the patients in the early death group when compared with 54.5%, 4.5%, and 22.7% of the patients in the late death group. Anterior pituitary infarcts were present in 10% of the patients with early deaths and 27.3% patients in the late death group. Hypothalamic hemorrhages were present in 44.4% of patients in early death and 78.6% in late death groups. Hypothalamic infarcts (40%) were present in the late death group only. Two patients (25%) in the early death group and 11 (84.6%) in the late death group had lesions in pituitary as well as hypothalamus (p < 0.05). CONCLUSIONS: Presence of ventricular compression on computed tomography scan and survival >24 hours after severe head injury has a significant correlation with the development of hypothalamic and pituitary lesions. Secondary insults account for a proportion of pituitary and hypothalamic lesions after trauma, which may be amenable to prevention by early intervention to treat raised intracranial pressure (ICP)/herniation.

[Paradoxal gazous embolism in hepatic trauma. Contribution of hyperbaric oxygenotherapy]. / Embolie gazeuse peropératoire chez un traumatisé hépatique. Intérêt de l'oxygénothérapie hyperbare.

A young man was admitted for a polytraumatism associating head trauma and blunt abdominal trauma with hepatic injury. He was managed with a damage control surgery with a perihepatic packing. During the second look surgery, he developed a paradoxal gazous embolism by air aspiration in the sus-hepatic vein. This has never been described before in such traumatism. The patient presented a respiratory distress, a circulatory shock due to right infarction and an intracranial hypertension with bilateral mydriasis. He was immediately treated by hyperbaric oxygenotherapy. The evolution was good and he recovered without sequelae.

Mannitol but not dantrolene prevents myocardial dysfunction following intra-cranial hypertension in rats.

Cardiac complications stemming from intra-cranial hypertension may result from impaired intra-cellular Ca(2+) homeostasis. The aim of this study was to examine the effects of dantrolene, a blocker of sarcoplasmic reticulum (SR) Ca(2+) release, on myocardial dysfunction associated with intra-cranial hypertension in rats. Dantrolene (10 mg) with and without 15% mannitol was administered to halothane-anesthetized rats prior to induction of intra-cranial hypertension by subdural balloon inflation. Its effects were compared to 3% and 15% mannitol and 5% Pentaspan. Dantrolene with mannitol or 15% mannitol alone prevented the transient intra-cranial hypertension-induced hyperdynamic response and ensuing circulatory collapse that was found in animals pre-treated with 3% mannitol solution or pentaspan. Moreover, hemodynamic function was preserved irrespective of TnI cleavage. However, only animals treated with high dose 15% mannitol exhibited lower lipid peroxidation content in the heart. In contrast, pre-treatment with dantrolene alone did not prevent the cardiac complications associated with intra-cranial hypertension. In conclusion, 15% mannitol attenuated the cardiopulmonary complications associated with intra-cranial hypertension. Dantrolene without mannitol was without effect. Since mannitol exhibits free radical scavenging properties, protection could be the result of a decrease in oxidative stress after intra-cranial hypertension.

[Abducens nerve palsy in spontaneous intracranial hypotension]. / Paralysie du nerf abducens secondaire à une hypotension intracrânienne spontanée.

Described by Schaltenbrand (1940), spontaneous intracranial hypotension is an unusual syndrome, sometimes revealed by an abducens nerve palsy motivating the patient to consult emergency ophthalmology services. The Authors report the case of a 50-Year-old Turkish woman who presented with diplopia due to a left abducens nerve palsy. These symptoms were associated with headache and nausea. Brain magnetic resonance imaging demonstrated diffuse pachymeningeal enhancement with gadolinium. A lumbar puncture showed low spinal fluid pressure (6 cm H2O), leading to the diagnosis of palsy by spontaneous intracranial hypotension. First, a classic treatment was prescribed with no result: increased water intake, corticoid therapy, and rest. Then a blood patch consisting of an injection of autologous blood by lumbar puncture between the third and fourth lumbar vertebrae to plug the spontaneous leak of spinal fluid, with success. A review of the literature provides information on the physiopathological mechanism, the clinical and imaging symptoms, and the treatment.

Ultrasonographic evaluation of optic disc swelling: comparison with CSLO in idiopathic intracranial hypertension.

PURPOSE: To determine the accuracy and reproducibility of ultrasonographic (US) readings of optic disc elevations in patients with papilledema compared with confocal scanning laser ophthalmoscope (CSLO) measurements. METHODS: One randomly selected eye of 22 patients with idiopathic intracranial hypertension (IIH) and a variable degree of optic disc swelling underwent five and three repeated measurements of disc height using high-resolution ultrasonography (Biovision unit; Quantel Medical, Clermont-Ferrand, France) and CSLO (Heidelberg Retina Tomograph [HRT]; Heidelberg Engineering, Heidelberg, Germany), respectively. The same procedure was assessed in 14 subjects with variable degrees of physiologic optic disc cupping. US and HRT measurements from each group were individually compared with each other to estimate the accuracy of US readings in both disc conditions in comparison with HRT data. RESULTS: Ultrasonographic readings were positively correlated with HRT measurements in both swollen (r = 0.62, P: = 0.002) and excavated disc (r = 0.84, P: < 0.0002). The 95% limits of agreement between the instruments were 0.24 +/- 0.59 mm (mean +/- 2 SD) and 0. 05 +/- 0.3 mm for swelling and cupping measurements, respectively. The coefficient of variation was 7.63% and 1.8% for swelling and 7. 93% and 5.91% for cupping, with US and HRT, respectively. CONCLUSIONS: The results indicate that US and CSLO readings are correlated i: both disc swelling and cupping conditions, but to a different extent because of a significant discrepancy in papilledema. US assessment can be considered highly reproducible. Combined US and HRT optic disc analysis may be recommended in papilledema evaluation as long as a better correlation can be demonstrated in further studies.