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Frederick A. Zeiler and Anthony M. Kaufmann

Repair of anterior skull base defects with vascularized grafts poses a significant challenge, given the location and small number of adequately sized vessels for free-flap anastomosis. This is particularly the case in the setting of redo surgery or in patients with preexisting soft-tissue trauma. Even more difficult is achieving a vascularized bone flap closure of such bony defects. The authors report a novel technique involving a rotational temporal bone flap with a temporalis muscle vascularized pedicle, which was used to repair an anterior fossa bony and soft-tissue defect created by recurrent malignancy.

A 55-year-old man with history of scalp avulsion during a motor vehicle accident, anterior fossa/nasopharyngeal malignant neuroendocrine carcinoma postresection, and bone flap infection presented with a recurrence of his skull base malignancy. The tumor was located in the anterior fossa, extending interhemispherically and down through the cribriform plate, ethmoid air cells, and extending into the nasopharyngeal cavity. Resection of the recurrent tumor was performed. The bony defect in the anterior skull base was repaired with a novel vascularized rotational temporal bone flap, with acceptable separation of the nasopharynx from the intracranial cavity.

The vascularized rotational temporal bone flap, in which a temporalis muscle pedicle is used, provides a novel and easily accessible means of vascularized bone closure of anterior skull base defects without the need for microsurgical free-flap grafting.

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Mark Gregory Bigder and Anthony M. Kaufmann


Microvascular decompression (MVD) surgery for hemifacial spasm (HFS) is potentially curative. The findings at repeat MVD in patients with persistent or recurrent HFS were analyzed with the aim to identify factors that may improve surgical outcomes.


Intraoperative findings were determined from review of dictated operative reports and operative diagrams for patients who underwent repeat MVD after prior surgery elsewhere. Clinical follow-up was obtained from the hospital and clinic records, as well as telephone questionnaires.


Among 845 patients who underwent MVD performed by the senior author, 12 had been referred after prior MVD for HFS performed elsewhere. Following repeat MVD, all patients improved and complete spasm resolution was described by 11 of 12 patients after a mean follow-up of 91 ± 55 months (range 28–193). Complications were limited to 1 patient with aggravation of preexisting hearing loss and mild facial weakness and 1 patient with aseptic meningitis without sequelae. Significant factors that may have contributed to the failure of the first surgery included retromastoid craniectomies that did not extend laterally to the sigmoid sinus or inferiorly to the posterior fossa floor in 11 of 12 patients and a prior surgical approach that focused on the cisternal portion of the facial nerve in 9 of 12 patients. In all cases, significant persistent neurovascular compression (NVC) was evident and alleviated more proximally on the facial root exit zone (fREZ).


Most HFS patients will achieve spasm relief with thorough alleviation of NVC of the fREZ, which extends from the pontomedullary sulcus root exit point to the Obersteiner-Redlich transition zone.

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Marshall F. Wilkinson and Anthony M. Kaufmann


Hemifacial spasm (HFS) is thought to be due to a hyperactive facial motor nucleus consequent to chronic neurovascular contact. The lateral spread (LS) response is presumed to reflect changes in facial motor neuron excitability. Facial muscle motor evoked potentials (MEPs) use the same efferent pathway as LS, therefore the authors speculated that these potentials should reflect differences consistent with changes at the facial motor nucleus level.


Monitoring of LS and bilateral facial MEP was performed in 10 consecutive patients undergoing MVD for HFS. Ipsilateral facial MEPs were monitored in 17 patients undergoing MVD for trigeminal neuralgia (TN). Latency, amplitude, and duration of the MEPs were compared before and after MVD.

Following MVD the duration of ipsilateral MEPs decreased from 17.6 ± 1.2 to 7.6 ± 0.7 msec and their amplitude decreased from 269.9 ± 66.3 to 76.5 ± 26.2 µV (p ≤ 0.01). These changes were consequent to the abolition of LS in eight of 10 patients and an approximately 50% reduction in two patients. The relationship between the reduction in MEPs and changes in LS was significant (p < 0.01). Control facial muscle MEPs (nonspastic side in patients with HFS and in those with TN) did not change significantly during the MVD procedure. Spasms were alleviated in nine of 10 patients, and there was no indication of facial nerve damage intraoperatively or postoperatively.


Facial muscle MEPs represent a novel tool for studying the neurophysiological mechanisms of HFS in particular and monitoring the facial nerve in general. Data in this study support the hypothesis that the development of HFS and its alleviation with MVD are related to changes in facial motor nucleus activity.

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Anthony M. Kaufmann and Angela V. Price

Peter Jannetta was a neurosurgery resident when he proposed the neurovascular compression theory. He built upon the astute observations of Dandy, Gardner, and others who, in the era before the operating microscope, had successfully ventured into the posterior fossa. In 1965, Jannetta performed cranial nerve microdissections for dental students and identified the trigeminal portio intermedia. He proposed that preservation of these sensory fibers may avoid complete facial numbness, and together with Robert Rand developed a subtemporal transtentorial approach for selective rhizotomy for trigeminal neuralgia (TN). Such rash surgery, using an operating microscope, was then forbidden at their University of California, Los Angeles center, so they collaborated with John Alksne to perform the first surgery at Harbor General Hospital. Upon visualizing the trigeminal nerve root, Jannetta was surprised to see a pulsating superior cerebellar artery compressing the nerve and said “That’s the cause of the tic.” He also hypothesized that alleviating the observed vascular cross-compression may be curative.

A few months later, while assessing a patient with hemifacial spasm, Jannetta had the epiphany that this was the same disease process as TN, but instead affecting the facial nerve. The patient consented to what would become Jannetta’s first microvascular decompression procedure. The senior faculty members who had forbidden such surgery were away, so the supervising neurosurgeon, Paul Crandall, granted the approval to perform the surgery and assisted. Via a retromastoid approach with the patient in the sitting position and using the operating microscope, Jannetta identified and alleviated the culprit neurovascular compression, with a cure resulting.

Jannetta presented his neurovascular compression theory and operative findings to the neurosurgical patriarchy of the time. Elders of the field were generally not inclined to accept the bold speculations of an untested neurosurgeon, and were often determined to discredit the new “cure” of the old diseases. Over decades of refining his surgical technique, documenting the outcomes, and enduring the skepticism he often faced, Jannetta’s theory and his microvascular decompression procedure withstood critical analysis and have become recognized as one the great discoveries and advances in neurosurgery and medicine.

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Marshall Wilkinson and Anthony M. Kaufmann

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Anthony M. Kaufmann and Erico R. Cardoso

✓ The authors investigated the pharmacokinetics of mannitol administered for treatment of vasogenic cerebral edema. A cortical cold injury was produced in 23 cats maintained under general anesthesia for 5 or 21 hours. Control animals received no mannitol, while treatment groups received either a single dose or five doses administered at 4-hour intervals of 0.33 gm/kg radiolabeled mannitol. Liquid scintillation counting was carried out to determine the concentrations of mannitol in the cerebral tissue, cerebrospinal fluid, plasma, and urine. Cerebral water content and linear progression of edema were also measured.

Rapid plasma clearance prevented accumulation of mannitol after multiple intravenous injections, as 84% ± 2% (mean ± standard error of the mean) of the infused mannitol was excreted through the urine. However, there was progressive accumulation of mannitol within the cerebral tissue, especially in the edematous white matter where it reached a level of 0.33 ± 0.03 mg/gm after five doses, exceeding the trough plasma concentrations by a ratio of 2.69:1. Water content measurement showed that a single dose of mannitol failed to reduce cerebral water content or edema progression at 4 hours postinjection, while multiple doses produced a 3% increase in water content in edematous regions (p > 0.0003). The results of this study demonstrated a reversal of the osmotic concentration gradient between edematous brain and plasma following multiple mannitol injections, associated with exacerbation of vasogenic cerebral edema.

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Andrew D. Firlik, Anthony M. Kaufmann, Charles A. Jungreis, and Howard Yonas

✓ In this study the authors have examined the effects of transluminal angioplasty on cerebral blood flow (CBF) in the management of intractable vasospasm following aneurysmal subarachnoid hemorrhage (SAH). Fourteen consecutively enrolled patients underwent attempted angioplasty with or without intraarterial infusion of papaverine. Twelve patients underwent pre- and postangioplasty xenon-enhanced computerized tomography (Xe-CT) scanning to measure regional CBF in 55 to 65 regions of interest (ROIs) per patient. Angioplasty was possible in 13 (93%) of 14 patients, with angiographically demonstrated improvement in all 13. Twelve (92%) of the 13 patients were neurologically improved following angioplasty; seven (58%) of the 12 patients who improved had a complete reversal of all delayed ischemic deficits. Angioplasty significantly decreased the mean number of ROIs at risk (11.4 ROIs pre- and 0.9 ROIs postangioplasty) (p < 0.00005, t-test). All patients had a reduction in the number of ROIs at risk after angioplasty; six (50%) of 12 no longer had any ROIs remaining at risk after angioplasty. Angioplasty significantly increased the mean CBF within at-risk ROIs (13 ml/100 g/minute pre- and 44 ml/100 g/minute postangioplasty) (p < 0.00005, t-test). All patients experienced an improvement in mean CBF in at-risk ROIs after angioplasty, with the mean CBF improving to above 20 ml/100 g/minute in all cases. No differences in the degree of improvement were found in patients who received intraarterial papaverine compared with those who did not. In the majority of patients with refractory vasospasm following SAH, angioplasty effectively dilated spastic arteries, reversed delayed neurological deficits, and significantly improved CBF in areas of brain at risk of infarction.

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Mauricio Campos-Benitez and Anthony M. Kaufmann


It is generally accepted that hemifacial spasm (HFS) is caused by pulsatile vascular compression upon the facial nerve root exit zone. This 2–3 mm area, considered synonymous with the Obersteiner–Redlich zone, is a transition zone (TZ) between central and peripheral axonal myelination that is situated at the nerve's detachment from the pons. Further proximally, however, the facial nerve is exposed on the pontine surface and emerges from the pontomedullary sulcus. The incidence and significance of neurovascular compression upon these different segments of the facial nerve in patients with HFS has not been previously reported.


The nature of neurovascular compression was determined in 115 consecutive patients undergoing their first microvascular decompression (MVD) for HFS. The location of neurovascular compression was categorized to 1 of 4 anatomical portions of the facial nerve: RExP = root exit point; AS = attached segment; RDP = root detachment point that corresponds to the TZ; and CP = distal cisternal portion. The severity of compression was defined as follows: mild = contact without indentation of nerve; moderate = indentation; and severe = deviation of the nerve course. Success in alleviating HFS was documented by telephone interview conducted at least 24 months following MVD surgery.


Neurovascular compression was found in all patients, and the main culprit was the anterior inferior cerebellar artery (in 43%), posterior inferior cerebellar artery (in 31%), vertebral artery (in 23%), or a large vein (in 3%). Multiple compressing vessels were found in 38% of cases. The primary culprit location was at RExP in 10%, AS in 64%, RDP in 22%, and CP in 3%. The severity of compression was mild in 27%, moderate in 61%, and severe in 12%. Failure to alleviate HFS occurred in 9 cases, and was not related to compression location, severity, or vessel type.


The authors observed that culprit neurovascular compression was present in all cases of HFS, but situated at the RDP or Obersteiner–Redlich zone in only one-quarter of cases and rarely on the more distal facial nerve root. Since the majority of culprit compression was found more proximally on the pontine surface or even pontomedullary sulcus origin of the facial nerve, these areas must be effectively visualized to achieve consistent success in performing MVD for HFS.