Lu et al from the United States report on cerebral salt wasting (CSW) and its causes after traumatic brain injury. The authors differentiated this from the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Cerebral salt wasting is the result of salt excretion in the urine. The excretion of salt water results in a lower blood volume, high hematocrit, low central venous pressure, and low serum sodium. The CSW is believed to be caused by the rise in brain natriuretic peptide (BNP) that causes salt excretion. The exact mechanism by which this peptide is released is not known. The article contains more details on these studies that are interesting, and it is the first to measure elevated BNP levels in patients with hyponatremia and CSW. The SIADH results from antidiuretic hormone secretion that retains water and thus lowers blood sodium, hematocrit, and serum urea nitrogen levels by dilution and expands blood volume. Urine sodiums are low. So, when we see patients who have hyponatremia, there can be 2 distinct causes. If fluid restriction is used, it will help patients with SIADH secretion and make those who have CSW worse. The authors describe their work identifying BNP as a cause of CSW and differentiate the syndromes. Paul Vespa, neurointensivist on the Editorial Board of Surgical Neurology, makes further editorial comments and discusses the treatment of hyponatremia in neurosurgical patients in this important new information for neurosurgeons. These are both nice articles to read and helpful in practice.
Holly et al from the United States report on an increasingly common problem seen by neurosurgeons—cervical myelopathy and cervical spinal stenosis in the elderly. Should cervical spinal decompressive surgery be performed on patients older than 75 years? Using both anterior and/or posterior approaches to the cervical spine in 36 patients, the authors compared the results of surgery in a group of patients older than 75 years (36 patients) with 34 patients younger than 65 years undergoing decompressive surgery for the same clinical and radiological picture. All presented with myelopathy. Both groups improved after surgery, the younger making better recoveries than the older group of patients. The elderly group had a higher rate of temporary complications (1/3 of the patients) than the younger group. The authors use the Modified Japanese Orthopedic Association scoring system in the article, which rates the motor performance in the upper and lower extremities, sensory deficits, and sphincter dysfunction, each on a scale of 0 to 4, with the highest scores meaning the best performance or no deficits. This is a nice study. Anterior and posterior surgery can be done on patients after the age of 75 years with success if they are selected properly. These patients can expect improvement even if wheelchair bound.
Tian et al from China report on a retrospective analysis of a consecutive series of 301 patients with traumatic subarachnoid hemorrhage (SAH). The authors were looking for factors leading to the development of hydrocephalus in these patients. They found hydrocephalus in 10% of their patients in follow-up. The hydrocephalus appeared related to the age of the patient, the presence of intraventricular hemorrhage, and the amount of subarachnoid blood present on initial imaging. Patients who have head injury can develop hydrocephalus that can be missed. The above factors should increase our suspicion that hydrocephalus will occur. However, a high index of suspicion by the neurosurgeon is important in recognizing hydrocephalus in patients who are post trauma.
Karasu et al from Turkey describe their experience with 65 patients who had traumatic epidural hematomas in the posterior fossa. This problem requires a high suspicion of its presence, imaging to prove its existence, and rapid surgical decompression as the authors describe. Ninety-five percent (95%) had occipital fractures, whereas 16 patients with small hematomas and no mass effect were observed.
Spontaneous spinal epidural hematoma (SSEH) is discussed in the literature, but there are few reports on large clinical series. Liu et al from China report on their management of 23 patients with SSEH. Nearly 80% had sudden neck or back pain, and nearly 10% presented with acute paraplegia. Magnetic resonance imaging showed either hypo-, iso-, or epidural hyperdensity at the site of the hematoma. Those with spinal cord edema on imaging had a worse prognosis. Almost 50% of SSEHs were found in the cervical or cervical-thoracic areas. For patients with an incomplete spinal cord injury, surgery was helpful. No cause was found in 60% of the cases, whereas vascular malformations were the second most common cause. This is a nice review of a large series of patients with SSEH.
Quigley et al from the United States analyzed their patients with aneurysmal SAH who were admitted with Hunt-Hess grades of 4 or 5. They placed a ventricular drain in all patients in anticipation that it would be needed. Basically, there were no predictors of outcome except the admission postventriculostomy or postclot evacuation Glascow Coma Score. The authors used immediate ventriculostomy, early operation, and triple H therapy for vasospasm. Forty-five percent (45%) of their grades 4 and 5 patients achieved a favorable outcome with a Glascow Outcome Score of 4 or 5. They recommend treating all aneurysmal SAH patients aggressively because there is no selective factor that distinguishes outcome.
Colli et al from Brazil have written an excellent article proposing a diagnostic surgical technique for nonmalignant inflammatory sensory polyganglioneuropathy (NISP), a rare neurological disorder. The NISPs are associated with carcinomas, Sjogren syndrome, or monoclonal gammopathies, or can be idiopathic. The patients present with sensory neuropathies; and by exclusion of other causes of the neuropathies, the diagnosis of NISP remains. Generally, as the authors state, there is no treatment of NISP; but responses have been reported to plasmaphoresis or steroid treatment. Before undertaking these treatments that have risk and expense, neurologists would like proof of their presumptive diagnosis of a ganglionopathy. The authors describe in detail the operative procedure to remove a sensory ganglion in the thoracic level as a diagnostic procedure. Read the article and the comments at the end. Offer this idea or send this article to your neurology colleagues. This is an excellent piece of work.
Lee et al from Taiwan present 15 patients with causalgia-like symptoms after a lumbar discectomy in a 1-year period. They treated their patients with computed tomographic–guided percutaneous chemical lumbar sympathectomies. Seventy-five percent (75%) of the patients had improvement of their symptoms, which lasted 24 months, the length of the study. Read Ron Pawl's comments at the end. “Does causalgia really exist?” he asks. Does reflex sympathetic dystrophy exist? Why do these authors have such a high incidence of this phenomenon after surgery? These symptoms and presumed disease are very troubling to the reader. We have all seen patients with the shinny sensitive skin and burning pain. The discussion refers to many hypotheses that are all unproven. What is going on in these patients? Is this a cultural phenomenon? I do not know the answers. Neither do our experts. What is your opinion?
Ohue et al from Japan report on the phenomenon of postoperative ischemic neurological deficits after direct or indirect revascularization in patients with moyamoya syndrome. The problem also exists in patients with atherosclerosis undergoing extracranial-intracranial bypass surgery or revascularization. This article is not easy to read. The important parts of this article are in the last 2 paragraphs of section 3.2, the case report, and in the discussion. Essentially, the authors recorded electroencephalograms, magnetic resonance images, and single photon emission computed tomographic images during these ischemic events in a few patients. They found no seizures but did discover hyperperfusion and increased fluid in the areas evaluated. So, they have provided an answer to this puzzling clinical picture seen after bypass surgery.
Westhout et al from the United States present an interesting case of neurosarcoidosis without enhancement of the meninges or elevation of cerebrospinal fluid angiotensin-converting enzyme levels as can be seen in central nervous system sarcoid. So, there were few clues to the diagnosis of sarcoid in this patient who presented with hydrocephalus. Read Cone's comments at the end. This is a very interesting case to remember.
Vilela from the United States reports on a case of “paradoxical herniation” of the brain. The patients all had craniotomies without bone replacement. Sometime after diagnostic lumbar punctures, the patients became somnolent. Because of a continuing lumbar cerebrospinal fluid leak after the lumbar puncture, downward brain herniation occurs without signs of increased intracranial pressure. This is a condition we should recognize. Read the article to learn about it.
Oshima et al from Japan report on a treatment of an external carotid aneurysm associated with Behcet disease. Behcet disease was described by a Turkish dermatologist. It is commonly found among Middle Eastern people and was once called the Silk Road Disease because of its prevalence along that route. It is believed to be caused by an overreaction of the immune system presumably producing inflammation of small blood vessels, ulcerations of the mouth and genitalia, uveitis, and skin lesions. Surgical grafting of aneurysmal dilatations formed in arteries is difficult because of pseudoaneurysm formation and thrombotic occlusion of the grafts. The authors used a coated endovascular stent to treat the aneurysmal dilatation of the carotid. The aneurysmal dilatation immediately resolved.
Boutarbouch et al from Morocco report a case of inflammatory extramedullary pseudotumor of the cervical spinal cord that presented as an epidural bleed. This is a rare lesion. The authors have reviewed the subject and made diagnostic and management recommendations.
Cohen et al report from Israel on an exsanguinating tracheoinnominate artery fistula at the site of a tracheostomy; find out what to do to stop the bleeding quickly.
Twelve years ago, I wrote an editorial for Surgical Neurology on “Who's life is it anyway?” It was about how physicians make decisions for their patients' lives that I think are not appropriate. I have republished that editorial because I continue to see the same problem existing today. If you have a life-threatening disease, do you want some consultant to tell you that there is no treatment or that they would not recommend treatment for you? Or do you just want the physician, as your consultant, to give you the options so that you can make your own decision? Read the editorial and see if it changes your mind.
I have also included another edition of Editor's Notes that contain items from the scientific, social, economic, and political world that I found interesting.
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