John L. D. Atkinson

Predictors of Cerebral Infarction in Aneurysmal Subarachnoid Hemorrhage

Background— Clinical and radiologic predictors of cerebral infarction occurrence and location after aneurysmal subarachnoid hemorrhage have been seldom studied. Methods— We evaluated all patients admitted to our hospital with aneurysmal subarachnoid hemorrhage between 1998 and 2000. Cerebral infarction was defined as a new hypodensity located in a vascular distribution on computed tomography (CT) scan. Results— Fifty-seven of 143 patients (40%) developed a cerebral infarction. On univariate analysis, occurrence of cerebral infarction was associated with a worse World Federation of Neurological Surgeons grade (P =0.01), use of ventriculostomy catheter (P =0.01), preoperative vasospasm (P =0.03), surgical clipping (P =0.02), symptomatic vasospasm (P <0.01), and vasospasm on transcranial Doppler ultrasonography (TCD) or repeat angiogram (P <0.01). On multivariable analysis, only presence of symptoms ascribed to vasospasm (P <0.01) and evidence of vasospasm on TCD or angiogram predicted cerebral infarction (P <0.01). TCD and angiogram agreed on the diagnosis of vasospasm in 73% of cases (95% CI, 63% to 81%), but the diagnostic accuracy of this combination of tests was suboptimal for the prediction of cerebral infarction occurrence (sensitivity, 0.72; specificity, 0.68; positive predictive value, 0.67; negative predictive value, 0.72). Location of the cerebral infarction on delayed CT was predicted by neurological symptoms in 74%, by aneurysm location in 77%, and by angiographic vasospasm in 67%. Conclusions— Evidence of vasospasm on TCD and angiogram is predictive of cerebral infarction on CT scan but sensitivity and specificity are suboptimal. Cerebral infarction location cannot be predicted in one quarter to one third of patients by any of the studied clinical or radiological variables.

Surgical treatment of spontaneous spinal cerebrospinal fluid leaks

OBJECT Spontaneous spinal cerebrospinal fluid (CSF) leaks are an increasingly recognized cause of intracranial hypotension and may require neurosurgical intervention. In the present report the authors review their experience with the surgical management of spontaneous spinal CSF leaks. METHODS Between 1992 and 1997, 10 patients with spontaneous spinal CSF leaks and intracranial hypotension were treated surgically. The mean age of the seven women and three men was 42.3 years (range 22-61 years). Preoperative imaging showed a single meningeal diverticulum in two patients, a complex of diverticula in one patient, and a focal CSF leak alone in seven patients. Surgical exploration in these seven patients demonstrated meningeal diverticula in one patient; no clear source of CSF leakage could be identified in the remaining six patients. Treatment consisted of ligation of the diverticula or packing of the epidural space with muscle or Gelfoam. Multiple simultaneous spinal CSF leaks were identified in three patients. CONCLUSIONS All patients experienced complete relief of their headaches postoperatively. There has been no recurrence of symptoms in any of the patients during a mean follow-up period of 19 months (range 3-58 months; 16 person-years of cumulative follow up). Complications consisted of transient intracranial hypertension in one patient and leg numbness in another patient. Although the disease is often self-limiting, surgical treatment has an important role in the management of spontaneous spinal CSF leaks. Surgery is effective in eliminating the headaches and the morbidity is generally low. Surgical exploration for a focal CSF leak, as demonstrated on radiographic studies, usually does not reveal a clear source of the leak. Some patients may have multiple simultaneous CSF leaks.

Hyperhidrosis: Evolving Therapies for a Well-Established Phenomenon

The socially embarrassing disorder of excessive sweating, or hyperhidrosis, and its treatment options are gaining widespread attention. In order of frequency, palmar-plantar, palmar-axillary, Isolated axillary, and cranlofacial hyperhidrosis are distinct disorders of sudomotor regulation. A common link among these disorders is an excessive, nonthermoregulatory sweat response often to emotional stimuli in body regions influenced by the anterior cingulate cortex as opposed to the thermoregulatory sweat response regulated by the preoptic-anterior hypothalamus. Diagnosis of these mechanistically ambiguous disorders is primarily from patient history and physical examination, whereas results of laboratory studies performed with indicator powder reveal the distribution and severity of resting hyperhidrosis and document the integrity of thermoregulatory sweating. Treatment options lie on a continuum based on the severity of hyperhidrosis and the risks and benefits of therapy. In general, therapy begins with antiperspirants or anticholinergics. Iontophoresis is available for palmar-plantar and axillary hyperhidrosis. Botulinum toxin type A or local excision/curettage is effective for isolated axillary hyperhidrosis not responsive to topical application of aluminum chloride. Endoscopic thoracic sympathectomy may be used for severe cases of palmar-plantar and palmar-axillary hyperhidrosis. No sole therapy of choice has emerged for craniofacial sweating. The long-term sequelae of hyperhidrosis and its treatment also are discussed.

Orthostatic headaches caused by CSF leak but with normal CSF pressures

Objective: To report that the syndrome of orthostatic headaches caused by CSF leak can be seen with persistently normal CSF pressures. Background: CSF leak or shunt overdrainage is known to cause orthostatic headaches and diffuse pachymeningeal gadolinium enhancement (DPGE), typically associated with unmeasurable or very low CSF pressures. Methods: Of 40 consecutive patients with orthostatic headaches and DPGE, all had low or unmeasurable CSF pressures, except seven patients who had consistently normal CSF pressures and are thus reported. All had undergone multiple CSF examinations. Results: Two patients had overdraining shunts, and five had documented CSF leaks. One refused treatment, but the other six patients responded to surgical treatment or epidural blood patch with complete resolution of symptoms and related MRI abnormalities. Conclusions: Some patients with symptomatic CSF leaks may have CSF opening pressures that are consistently within normal limits. In the presence of convincing clinical features and imaging abnormalities, a normal CSF pressure should not discourage the clinician from searching for a source of CSF leak.

Preliminary Comparison of the Endoscopic Transnasal vs the Sublabial Transseptal Approach for Clinically Nonfunctioning Pituitary Macroadenomas

OBJECTIVE To assess the advantages and disadvantages of an endoscopic transnasal approach to pituitary surgery for a select group of clinically nonfunctioning macroadenomas and to compare results of this approach with the sublabial transseptal approach at a single institution. PATIENTS AND METHODS We retrospectively reviewed the records of 26 patients with clinically nonfunctioning pituitary macroadenomas approached endoscopically and 44 matched control patients with the same tumors approached sublabially between January 1, 1995, and October 31, 1997. RESULTS At baseline, the groups were not significantly different for age, sex distribution, number of comorbid conditions, visual field defects, degree of anterior pituitary insufficiency, or preoperative assessment of tumor volume or invasiveness. Mean (SD) operative times were significantly reduced in the endoscopic group vs the sublabial group: 2.7 (0.7) hours vs 3.4 (0.9) hours (P < .001). Postoperative assessment of surgical resection and postoperative alterations of anterior pituitary function or visual fields were not significantly different between groups, and complication rates were similar in both groups. CONCLUSION This endoscopic transnasal approach to pituitary resection results in significantly shorter operative time without compromising the extent of tumor resection. The distinct disadvantage of this approach is an off-center view of the sella and a diminished working channel to the sella turcica. For these reasons, the endoscopic approach or its variation is an alternative to the sublabial approach but should be considered only by experienced pituitary neurosurgeons.

Second Impact Syndrome: Concussion and Second Injury Brain Complications

P A C a t t m p e p R b e econd impact syndrome was first described in 1973 by ichard Schneider in 2 young athletes who experienced nitial concussive syndromes and subsequently died after a elatively minor second head injury. Saunders and Haraugh coined the term second impact syndrome in their 984 description of a 19-year-old college football player ho suffered a head injury with brief loss of consciousness, eturned to play, reported a headache, and on the 4 day ollapsed, became unresponsive, and died. Postmortem xamination revealed no space-occupying hematoma and xtensive cerebral edema. It is the second collision impact, bsence of space-occupying hematoma, and subsequent apid and profound brain swelling that identify and mark he second impact syndrome. The severe brain swelling and bsence of impact hematoma are identical to first head njury findings duplicated in head injury laboratory nvestigations and identified in clinical series of severe ead injury patients. Statistics as to the occurrence of second impact synrome do not exist and the actual prevalence and incidence emain unknown. Second impact syndrome has always had roponents and detractors. Multiple head injury experts ave discussed this phenomenon as a worrisome corollary n virtually every article or chapter on sport-related head njury. However, others have been suspicious that the ure form is rare, and some have called into question its xistence, commenting “. . . it is fear of this entity that nderpins concussion guidelines regarding return to port.” The latter statement prompted a strong rebuttal rom a long-term and fully fledged head injury investigator ho noted that, although the syndrome might be uncomon, its existence is a reality and is identifiable at some evel virtually every year. In addition, it would be naïve to uggest return to play guidelines are solely in place as a onsequence of possible second impact syndrome, when here are multiple reasons to protect a concussed athlete rom re-exposure to play too early. Second impact synrome is only a small determinant for return to play guide-

Radiation-associated atheromatous disease of the cervical carotid artery: report of seven cases and review of the literature

The natural history of postirradiation extracranial cerebrovascular disease is uncertain. Previous reported cases spanning 20 years of carotid surgery are difficult to evaluate, because patients may sometimes have unspecified symptoms, physical examinations, postoperative results, and follow-up. Also, the evolution of carotid surgery over the past two decades makes it impossible to compare earlier operative technique with the state-of-the-art technique of today. Our series of 7 patients underwent 9 carotid endarterectomies with an average follow-up period of 46 months. The number of patients is small, and although technically this is a more difficult operation, we feel the results are favorable and may be comparable with endarteerctomy procedures in nonirradiated patients. These patients should be approached as if radiation changes are not a major factor when they are considered for reconstructive arterial surgery.

Neuroimaging in Deteriorating Patients With Cerebellar Infarcts and Mass Effect

Background and Purpose The decision to proceed with surgery in cerebellar infarct with mass effect (CIMASS) in deteriorating patients is based on clinical features. The potential role of neuroimaging in predicting deterioration has not been systematically studied. In this study we determine the role of neuroimaging in predicting deterioration in CIMASS. Methods We retrospectively reviewed the clinical and neuroimaging features in 90 patients with cerebellar infarcts. We selected for detailed analysis CIMASS in 35 patients. Results Eighteen patients remained stable and 17 deteriorated. Of these 17 patients, 8 were treated conservatively and 9 had surgery. Radiological features indicative of progression were more common in deteriorating patients compared with stable patients: fourth ventricular shift (82.3% versus 50%, P =0.075, OR=4.67), hydrocephalus (76.5% versus 11.1%, P =0.0001, OR=26), brain stem deformity (47% versus 5.6%, P =0.0065, OR=15.1), and basal cistern compression (35.3% versus 0%, P =0.0076, OR=20.91). Differences in upward displacement of the aqueduct and pontomesencephalic junction from Twining’s line, tonsillar descent on sagittal MRI, and infarct volumes between stable and deteriorating patients were not statistically significant. Conclusions Hydrocephalus, brain stem deformity, and basal cistern compression may herald deterioration in CIMASS. Admission to a neurological-neurosurgical intensive care unit and consideration of preemptive surgery are warranted in these patients. Vertical displacement of tonsils or aqueduct, demonstrated by MR imaging, did not predict deterioration.

The effect of carbon dioxide on the diameter of brain capillaries

Cerebral capillaries in cats subjected to variations in carbon dioxide tensions were studied using carbon black perfusion fixation. Five animals each were grouped into hypocapnia, normocapnia, and hypercapnia and 500 cortical, 250 white matter and 250 caudate nucleus capillaries per group were analyzed at 400 x magnification. Capillary diameters were found to change significantly in the cortex (6.1-10.0 microns), white matter (6.5-9.6 microns) and caudate nucleus (6.3-8.8 microns) from hypocapnia to hypercapnia, respectively. These findings suggest that capillary vasomotion occurs and that capillaries are not rigid tubes as previously portrayed.

Absent pachymeningeal gadolinium enhancement on cranial MRI despite symptomatic CSF leak

Article abstract CSF leak is recognized to cause orthostatic headaches and diffuse pachymeningeal gadolinium enhancement (DPMGE) on MRI. We report six patients with typical symptoms and documented CSF leaks without DPMGE. Two had normal meninges from the onset; one initially had normal meninges, but subsequently DPMGE developed. In three, the initially noted DPMGE resolved while they were still symptomatic with documented continued CSF leaks. Absent DPMGE does not rule out CSF leak. When clinical manifestations suggest this disorder, additional diagnostic studies should be pursued.