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Ramin Eskandari, Michael R. Filtz, Gary E. Davis and Robert E. Hoesch

Object

Normal intracranial pressure (ICP) and cerebral perfusion pressure (CPP) have been identified as favorable prognostic factors in the outcome of patients with traumatic brain injuries (TBIs). Osmotic diuretics and hypertonic saline (HTS) are commonly used to treat elevated ICP in patients with TBI; however, sustained effects of repeated high-concentration HTS boluses for severely refractory ICP elevation have not been studied. The authors' goal in this study was to determine whether repeated 14.6% HTS boluses were efficacious in treating severely refractory intracranial hypertension in patients with TBI.

Methods

In a prospective cohort study in a neurocritical care unit, adult TBI patients with sustained ICP > 30 mm Hg for more than 30 minutes after exhaustive medical and/or surgical therapy received repeated 15-minute boluses of 14.6% HTS over 12 hours through central venous access.

Results

Response to treatment was evaluated in 11 patients. Within 5 minutes of bolus administration, mean ICP decreased from 40 to 33 mm Hg (30% reduction, p < 0.05). Intracranial pressure–lowering effects were sustained for 12 hours (41% reduction, p < 0.05) with multiple boluses (mean number of boluses 7 ± 5.5). The mean CPP increased 22% and 32% from baseline at 15 and 30 minutes, respectively (p < 0.05). The mean serum sodium level (SNa) at baseline was 155 ± 7.1 mEq/L, and after multiple boluses of 14.6% HTS, SNa at 12 hours was 154 ± 7.1 mEq/L. The mean heart rate, systolic blood pressure, blood urea nitrogen, and creatinine demonstrated no significant change throughout the study.

Conclusions

The subset of TBI patients with intracranial hypertension that is completely refractory to all other medical therapies can be treated effectively and safely with repeated boluses of 14.6% HTS rather than a one-time dose.

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Ron Ron Cheng, Ramin Eskandari, Cynthia T. Welsh and Abhay K. Varma

Peripheral nerve involvement may be the first sign of systemic amyloid light-chain (AL) amyloidosis, a rare disease. Physical examination and electrodiagnostic testing are the mainstays of peripheral neuropathy evaluation at presentation. Sural nerve biopsy is performed in conjunction with serum and urine protein evaluation to differentiate between focal and systemic disease. Systemic disease is treated with a combination of chemotherapy, steroids, and stem cell transplantation. Isolated peripheral nerve disease is extremely rare.

The authors here report the case of an 80-year-old woman who presented with progressive right upper-extremity weakness due to right radial neuropathy discovered upon electrodiagnostic testing. Magnetic resonance neurography (MRN) revealed a focal lesion within the right radial nerve. She underwent radial nerve exploration and excision of an intraneural mass consisting of amyloid on histopathology, with mass spectrometry analysis diagnostic for AL amyloidosis. Noninvasive testing and clinical history did not suggest systemic involvement. This unique case of isolated peripheral nerve AL amyloidosis in the absence of signs and symptoms of systemic disease is described, and the literature demonstrating peripheral nerve involvement in AL amyloidosis is reviewed.

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Ramin Eskandari, James P. McAllister II, Janet M. Miller, Yuchuan Ding, Steven D. Ham, David M. Shearer and John S. Way

Object. The authors of previous studies have suggested that connectivity within the cerebral cortex may be irreversibly altered by hydrocephalus. To examine connectivity-related changes directly, the authors conducted a study in which they used an axonal tracer in an animal model of infantile hydrocephalus.

Methods. In five hydrocephalic kittens low-pressure ventriculoperitoneal (VP) shunts were placed 10 to 14 days after induction of hydrocephalus by intracisternal kaolin injections. Wheat germ agglutinin-conjugated horseradish peroxidase was injected laterally into the motor cortex in hydrocephalic animals 9 to 15 days after kaolin injection, and 1, 2, and 4 weeks after VP shunt insertion in shunt-treated animals, and in age-matched controls.

Reduction of antero- and retrograde labeling was most profound within the contralateral cortex and portions of the midbrain. Thalamic nuclei exhibited reductions in anterograde and retrograde labeling. Labeling within cell bodies of the ventral tegmental area decreased greatly in animals with untreated hydrocephalus, in which retrograde labeling was reduced in the locus coeruleus but did not affect the raphe nucleus. Shunt treatment increased both antero- and retrograde labeling of contralateral motor cortex to near-normal levels. Thalamic relay nuclei recovered antero- and retrograde labeling, although not to levels exhibited in controls. Shunt therapy restored cellular labeling within the ventral tegmental area and locus coeruleus. Recovery of labeling occurred as early as 7 days after shunt insertion.

Conclusions. Collectively, analysis of these data indicates the following. 1) Cortical connectivity involving both afferent and efferent pathways was impaired in untreated hydrocephalic animals. 2) Shunt therapy improved both cortical afferent and efferent connectivity. 3) Complete reestablishment of the cortical efferent pathways, however, did not occur. Cortical pathway dysfunction, if permanent, could cause many of the motor and cognitive deficits seen clinically in children with hydrocephalus.