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Observations on synkinesis in patients with hemifacial spasm

Effect of microvascular decompression and etiological considerations

Phyo Kim and Takanori Fukushima

✓ In 95 patients with hemifacial spasm, synkinetic actions were measured objectively using electromyographic examination of the blink reflex and impedance audiometry. Abnormal synkinesis between the orbicularis oculi and the orbicularis oris muscles was recorded in 93% of cases, while synkinesis between the stapedius muscle and the facial muscles was recorded in 87%. Neither of these effects could be demonstrated on the unaffected side. The examinations were performed before and after microvascular decompression in 66 cases. Rapid disappearance of synkinesis, often within 10 days, was observed after the relief of vascular compression in 81% of patients who had not undergone previous peripheral facial nerve block procedures. These findings indicate that the synkinesis seen in hemifacial spasm is essentially a reversible condition, and suggest that axonal ephaptic conduction at the vascular compression site plays an important role in the pathophysiological mechanism of hemifacial spasm.

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Shinji Yamamoto, Hideaki Kanaya and Phyo Kim


Spinal digital subtraction angiography (DSA) is indispensable for the precise diagnosis of spinal vascular lesions and the assessment of blood supply to the spinal cord. However, comprehensive spinal DSA covering multiple segments requires repetition of selective catheterization into small segmental arteries, which is time consuming, sometimes difficult, and hazardous. The authors investigated the usefulness of CT angiography with intraarterial contrast injection (IA-CTA) as a preliminary study preceding spinal DSA. With the advent of multidetector CT, it is feasible to obtain images of the spinal cord vasculature instantaneously overa number of segments.


A total of 56 patients with lesions involving the spinal vasculature underwent IA-CTA with 64- or 320-row detector CT in advance of comprehensive spinal DSA. Contrast material was injected via a pigtail catheter placed at the aorta in proximity to the segments of interest. Scanning was repeated twice to obtain arterial- and venous-phase images to differentiate between the arterial and venous components. The spinal arteries were identified by paging the various multiplanar reconstruction images and tracing the vessels from the aorta. Spinal DSA was subsequently performed by guiding selective catheterization to the feeding segments in reference to the IA-CTA findings. Visualization of the segmental arteries, normal spinal arteries, and abnormal vessels during IA-CTA was investigated and compared with that obtained during spinal DSA.


In all 56 patients, spinal IA-CTA successfully enabled visualization of the spinal vessels, including the radicular arteries and the anterior spinal artery. Below the aortic arch, all segmental arteries were identified clearly. The segmental arteries, radiculomedullary arteries, spinal arteries, and abnormal vessels were traced from the aorta, which would be the target of selective catheterization. In 3 (6.8%) patients, IA-CTA revealed severe aortic atherosclerosis and occlusion of some segmental arteries. The information obtained was useful for directing selective catheterization studies. The findings of IA-CTA corresponded well with those of spinal DSA.


IA-CTA is a useful adjunct to spinal DSA for surveying the vasculature surrounding the spinal cord and for orienting selective catheterization. IA-CTA can complement spinal DSA, curtail unnecessary segmental injections, and thus reduce procedural complications.

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Shinji Yamamoto, Ryu Kurokawa and Phyo Kim


Regional blood flow is decreased in experimental models of chronic spinal cord compression, and the alteration presumably contributes to the development of myelopathy. Cilostazol (Otsuka Pharmaceuticals Co.), a selective Type III phosphodiesterase inhibitor, has been shown to be neuroprotective in cerebral hypoperfusion animal models and clinically effective in preventing the recurrence of cerebral infarction. To investigate the neuroprotective effect of cilostazol on cervical spondylotic myelopathy, the preventive effect against progressive motor dysfunction and the loss of anterior horn motor neurons were assessed using a chronic cord compression model in rats.


To produce chronic cervical cord compression in male Wistar rats, thin polyurethane sheets (3 × 5 × 0.7 mm) that gradually expand over 48–72 hours by absorbing water were implanted under the C5–6 laminae. In sham operations, the sheets were momentarily placed and then immediately removed. This model has been shown to reproduce characteristic features of clinical cervical myelopathy, with progressive motor disturbances after a latency period and insidious neuronal loss preceding the onset of symptoms. In the treatment group, cilostazol (30 mg/kg/day) was orally administered to the rats once a day, starting the day after surgery and continuing through the entire observation period of 25 weeks. In the control group, vehicle solution was administered under the same protocol. Changes in motor function were monitored by measuring bilateral forepaw grip strength and the duration of forced running on a treadmill. Twenty-five weeks after surgery, cervical spinal cords were examined histopathologically.


Cilostazol preserved both forepaw grip strength and forced running capability. The drug also preserved anterior horn motor neurons in the C5–6 spinal cord segment, which diminished in number in the untreated chronic compression group. The drug decreased the number of TUNEL-positive apoptotic cells.


These results indicate that cilostazol is neuroprotective in the chronically compressed cervical cord and is potentially useful in the treatment of cervical spondylotic myelopathy.

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Yuhei Yoshimoto, Phyo Kim, Tomio Sasaki and Kintomo Takakura

✓ To investigate the pathogenetic significance of metabolic failure observed in spastic cerebral arteries after subarachnoid hemorrhage (SAH), the temporal profile of alterations in the arterial content of high-energy phosphates was studied. A canine model of double hemorrhage was used. Constriction of the basilar artery was measured angiographically on Days 3, 5, 7, and 14 after SAH in separate groups of animals. Adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), guanosine triphosphate (GTP), guanosine diphosphate, creatine phosphate (CrP), and creatine (Cr) levels in the arteries were assayed using high-performance liquid chromatography. A time-dependent development of angiographic spasm was confirmed. A mild vasospasm was seen in the group studied 3 days after SAH, progressed in the Day 5 group, remained comparably severe in the Day 7 group, and resolved partially in the Day 14 group. The content of high-energy phosphates (ATP, GTP, and CrP) declined rapidly over the course of the study, and a significant reduction in ATP, GTP, and CrP was observed in the Day 3 group. Levels of ATP and CrP decreased further in the Day 5 and 7 groups. The decrement in GTP was completed in the early phase; a significant reduction took place in the Day 3 group, with no progression thereafter and no recovery though Day 14. Total adenylate (ATP + ADP + AMP) and total creatine (Cr + CrP) content diminished markedly over the course of the study. These results indicate that metabolic failure and trophic disturbance in the cerebral artery occurs with a rapid onset following SAH and progresses in close association with the development of vasospasm, suggesting a significant causal relationship with the pathogenesis.

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Phyo Kim, James D. Jones and Thoralf M. Sundt Jr.

✓ High-energy phosphate levels were measured in the canine cerebral artery during chronic vasospasm. Subarachnoid hemorrhage and vasospasm were induced by percutaneous injections of autologous venous blood into the cisterna magna. Narrowing of the artery was confirmed by angiography 7 days later. Levels of adenosine phosphates (adenosine triphosphate (ATP), adenosine diphosphate (ADP), and adenosine monophosphate (AMP)), guanosine phosphates (guanosine triphosphate (GTP) and guanosine diphosphate (GDP)), and creatine phosphate (CrP) in the basilar artery were quantified using high-performance liquid chromatography. The total creatine (Crtotal) content was measured by a spectrophotometric method after acid hydrolysis of CrP. Levels of ATP, GTP, and CrP were markedly reduced in the spastic arteries, and ratios of ATP:ADP, GTP:GDP, and CrP:Crtotal were significantly decreased. The results indicate a serious disturbance in the energy metabolism that takes place in the cerebral artery during chronic vasospasm.

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Phyo Kim, Thoralf M. Sundt Jr. and Paul M. Vanhoutte

✓ The purpose of this study was to examine the hypotheses that structural stiffening of the arterial wall contributes to chronic cerebral vasospasm, and that alteration in properties of smooth muscle takes place after subarachnoid hemorrhage (SAH). Subarachnoid hemorrhage and subsequent chronic vasospasm were induced in dogs by two cisternal injections of autologous blood (on Day 0 and Day 2). Vasospasm was confirmed by angiography performed on Day 0 and Day 7. Animals in the control group underwent angiography only. On Day 8, the mechanical properties of the basilar arteries were studied in vitro. Passive compliance, measured under total inhibition of spontaneous myogenic tone with diltiazem (10−4 M) plus papaverine (10−4 M) was smaller in the SAH group. The length-contraction curve was shifted to the left and the optimum length for maximum contraction (Lmax) was significantly shorter in the spastic blood vessels. The spontaneous myogenic tone was augmented in the SAH group, resulting in an increase in resting tension at each length. By contrast, the maximum contractions in response to KCl and uridine 5′-triphosphate were markedly reduced in the SAH group, without changes in sensitivity to these agents. These differences in mechanical properties were observed in rings both with and without endothelium. The results indicate that, in chronic vasospasm, stiffening of the noncontractile component of the vasculature takes place as well as alterations in the contractile component, both of which presumably contribute to the shift in resting length-tension relationship and length-contraction relationship of the artery. The decreased distensibility, the increase in resting tension, and the shortening of the Lmax all favor a smaller diameter of the artery after SAH, possibly contributing to vasospasm.

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Yuhei Yoshimoto, Phyo Kim, Tomio Sasaki, Takaaki Kirino and Kintomo Takakura

✓ The present study was undertaken to determine whether oxyhemoglobin (OxyHb) is responsible for the functional alterations in the cerebral arteries observed during chronic vasospasm after subarachnoid hemorrhage. Vascular strips of canine basilar arteries were kept in organ culture for 3 days with or without repetitive exposure to OxyHb (OxyHb-treated and control strips). Contractions elicited by high levels of potassium (80 mM) and uridine 5′-triphosphate (3 × 10−4 M) were reduced in the OxyHb-treated group in a concentration-dependent manner. The relaxations evoked by nitric oxide and 8-bromo-cyclic guanosine monophosphate (8-bromo-cGMP) were not affected. Relaxations elicited by the calcium channel blocker, diltiazem, were attenuated in the OxyHb-treated rings. When the extracellular calcium concentration ([Ca++]e) was changed from a concentration in the external solution of 10−8 M to 10−3 M, myogenic tension developed. Myogenic tension, expressed as a percentage of the maximum contraction in each segment, was augmented in the OxyHb-treated group at [Ca++]e of 10−5 M and 10−4 M. There were no significant differences in passive compliance of the arterial wall between the two groups. These results demonstrated that prolonged exposure to OxyHb in vitro results in a decrease in contractile capacity and an increase in sensitivity to [Ca++]e, in agreement with previous findings in spastic arteries. By contrast, impairment of the 8-bromo-cGMP—mediated relaxation pathway and increased stiffness of the arterial wall, which have been reported to occur in spastic arteries, were not induced by prolonged exposure to OxyHb in vitro.

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Phyo Kim, Thoralf M. Sundt Jr. and Paul M. Vanhoutte

✓ To investigate the alteration of endothelium-dependent responses in chronic vasospasm after subarachnoid hemorrhage (SAH), experiments were carried out in the double-hemorrhage canine model. After the presence of vasospasm was confirmed by cerebral angiography on Days 0 and 7, pharmacological studies on the basilar artery were conducted in vitro on Day 8. In the SAH group, endothelium-dependent relaxation was abolished in response to arginine vasopressin and was significantly reduced in response to thrombin. Endothelium-independent relaxation in the SAH group was preserved in response to papaverine and was minimally reduced in response to sodium nitroprusside. Endothelium-dependent contraction in response to arachidonic acid, acetylcholine, the calcium ionophore A23187, adenosine diphosphate, mechanical stretching, and hypoxia persisted in the SAH group. The maximal contraction to KCl and uridine triphosphate, which is endothelium-independent, was diminished in the SAH group, but no changes in sensitivity were noted in the concentration-response relationships. A significant correlation was observed between the degree of vasospasm determined angiographically and the loss of endothelium-dependent relaxation. The loss of endothelium-dependent relaxation and the persistence of endothelium-dependent contraction suggest that the deterioration in the endothelium-dependent responses may be an important component in the pathogenesis of cerebral vasospasm.

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Phyo Kim, Buichi Ishijima, Hiroshi Takahashi, Hiroyuki Shimizu and Masayuki Yokochi

✓ The case is reported of a patient with progressive left hemiparesis due to vascular compression of the medulla oblongata. Metrizamide computerized tomography cisternography revealed that the left vertebral artery was compressing and distorting the left lateral surface of the medulla. Compression was surgically relieved and symptoms improved postoperatively. Neurological and symptomatic considerations are discussed in relation to the topographical anatomy of the lateral corticospinal tract.

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Phyo Kim, Susumu Wakai, Seigo Matsuo, Takashi Moriyama and Takaaki Kirino

Hydroxyapatite (HA) is the main constituent of bone mineral, and synthetic HA serves as a biocompatible and bioactive material. It permits bone growth on its surface and forms a union with the adjacent bone.

Object. The authors have developed implants made of porous HA, which they have used in more than 90 cases in the past 6 years to achieve cervical interbody fusion. The implants were designed to provide maximum durability, biomechanical stability, and alignment preservation and to be technically easy to use. The authors summarize their experience and results with the use of these implants.

Methods. The results of postoperative follow-up observation of 12 months or longer (mean 37.1 ± 2.4 months) are available in 70 patients with underlying disease including: spondylosis, disc extrusion, ossification of the posterior longitudinal ligament (PLL), hypertrophy of the PLL, and trauma. The patients' ages at the time of surgery ranged from 22 to 83 years (mean 50.6 ± 1.3 years).

Flexion—extension radiographs and tomograms, obtained 6 and 12 months after surgery and every year thereafter, were used to demonstrate solid fusion in all cases. Dislocation of the implant occurred in three patients who were treated during the early portion of the series. At 6 to 12 months after surgery, encasement of the implant and formation of union were observed. Normal lordosis, if present prior to surgery, was maintained postsurgery. No neurological deterioration related to the site of fusion occurred during the period of observation.

Conclusions. The authors conclude that satisfactory interbody fusion can be achieved by using HA implants, provided their design is appropriate and adequate surgical techniques are used.