Temporomandibular joint reconstruction after failed teflon-proplast implant: case report and literature review.

Multiple reports document that a foreign-body giant cell reaction forms around Proplast-Teflon temporomandibular joint (TMJ) implants. This results in destruction of surrounding bone and instability of the implants. This case presents a patient whose Proplast-Teflon TMJ implants became displaced into her middle cranial fossa. The staged reconstruction of this patient is described, including removal of the TMJ implants, reconstruction of the defect, concomitant orthodontic treatment and final reconstruction with TMJ Concepts. This process involved a multidisciplinary approach between several medical and dental specialties. At her 3-year follow up, the patient had a stable postoperative result.

Simultaneous Bilateral Vertebral Artery 3D Rotational Angiography. Technical Report of Two Cases.

SUMMARY: We describe the first reported use of simultaneous bilateral vertebral artery rotational angiography to visualize an aneurysm. Images acquired from 3D rotational angiography with a single vertebral injection provided insufficient anatomic detail in two cases with vertebrobasilar junction aneurysms associated with fenestration. Therefore, simultaneous bilateral vertebral artery 3D rotational runs were performed. Anatomic detail was superior with the simultaneous injection and this allowed for the appropriate plan of care to be instituted. In the rare cases of vertebrobasilar junction aneurysm associated with fenestration, simultaneous bilateral vertebral artery 3D rotational angiography may provide the most useful anatomic detail when evaluating a patient for possible endovascular intervention.

Transcranial Doppler identification of changing autoregulatory thresholds after autoregulatory impairment.

OBJECTIVE: Transcranial Doppler (TCD) flow velocity (FV) assessment may provide a useful index of autoregulatory impairment after severe head injury. It may define a therapeutic end point against which cerebral perfusion pressure (CPP) can be titrated. This study examines the relationship between cerebral blood flow (CBF) and TCD FV indices in a laboratory model before and after autoregulatory impairment. METHODS: CPP, CBF, and middle cerebral artery TCD FV were measured continuously in nine anesthetized and ventilated sheep. CPP was decreased by hemorrhagic hypotension. The process was repeated after impairment of autoregulation by cisternal infusion, which maintained CPP at 0 mm Hg for 15 minutes. Points of significant change (i.e., breakpoints) from baseline values for each of the measured flow parameters were identified by using a ratio of variance technique. RESULTS: Before any significant change in CBF or systolic TCD, diastolic TCD FV decreased (mean breakpoint, 69 mm Hg; range, 56-78 mm Hg) as CPP was reduced. This divergence of diastolic and systolic TCD FV, which occurred before autoregulatory failure, was associated with an increasing TCD pulsatility index (mean breakpoint, 63 mm Hg; range, 53-70 mm Hg). At diastolic TCD FV congruent with 10 cm/s, systolic TCD FV (mean breakpoint, 48 mm Hg; range, 46-53 mm Hg) and CBF (mean breakpoint, 49 mm Hg; range, 47-51 mm Hg) decreased rapidly, indicating autoregulatory failure. After autoregulatory impairment, the breakpoints for all four indices shifted to higher CPP values (mean, 16 mm Hg). CONCLUSION: TCD FV assessment identified two CPP thresholds of autoregulatory loss. Before autoregulatory failure, an earlier phase of autoregulatory disturbance may be detected by divergent systolic and diastolic TCD FVs. It is important to note that this phase may be detected before CBF decreases. These TCD FV breakpoints depend on the state of autoregulatory impairment and may provide potential targets for CPP-directed therapy.

Mannitol for resuscitation in acute head injury: effects on cerebral perfusion and osmolality.

OBJECTIVE: To review the use of mannitol during initial resuscitation following traumatic brain injury and to determine the effects of mannitol on subsequent management following resuscitation and commencement of neuromonitoring. METHODS: A retrospective audit of patients presenting to a tertiary hospital with severe head injury (Glasgow coma score < or = 8). Patients were divided into two groups according to whether they received mannitol during initial resuscitation. Measurements included initial plasma osmolality, cerebral perfusion pressure (CPP), intracranial pressure (ICP) and jugular venous saturation (SjO2). RESULTS: Forty patients were identified: 19 received mannitol prior to admission to the intensive care unit. Of these, only 2 patients fulfilled acceptable neurological indications for mannitol. The mannitol patients received a mean dose of 237 mL of 20% mannitol (47.4 g) and had significantly higher initial osmolalities than the patients who did not receive mannitol (293 vs 279 mosmol/L, p < 0.05). No significant difference in initial CPP, ICP, or SjO2 was identified. The mannitol patients were further subdivided into two 12-month periods (1994 and 1995). A dose related, significant difference in initial osmolalities was identified (140 vs 344 mL and 284 vs 304 mosmol/L respectively, p < 0.05). The latter group (n = 9) had significantly lower initial CPPs (72 vs 59 mmHg) and higher ICPs (14 vs 18 mmHg). No difference in 6 month Glasgow outcome scores between groups was demonstrated. CONCLUSIONS: The empirical overuse of mannitol is common. Mannitol did not exert any beneficial effect on CPP, ICP or SjO2 in the initial phases of management. Larger doses (i.e. > 20 g) are associated with increased osmolality which may reduce CPP.

Transcranial Doppler assessment of the lower cerebral autoregulatory threshold.

Continuous transcranial Doppler ultrasonography of the middle cerebral artery (TCD-MCA) has been proposed as a method of identifying the lower cerebral autoregulatory threshold. This study investigated the relationship between continuous TCD-MCA and cerebral blood flow (CBF) in sheep. Arterial blood pressure, intracranial pressure, CBF and left TCD-MCA were measured in 12 anaesthetized and ventilated merino sheep. Cerebral perfusion pressure (CPP) was reduced by haemorrhagic hypotension. Measurements were recorded continuously and breakpoint thresholds calculated by an analysis of variance. The TCD-MCA systolic velocity breakpoint (50 +/- 1.5 mmHg) did not significantly differ from the lower limit of autoregulation, identified by the CBF breakpoint (50 +/- 1.8 mmHg). The TCD-MCA diastolic velocity breakpoint occurred at a significantly higher level of CPP (64 +/- 2 mmHg) (P < 0.01). The relationship between TCD-MCA flow velocity and CBF thresholds has been described. Early divergence of flow velocity may represent a compensatory mechanism to maintain CBF.

Widespread early dendritic injury associated with loss of cortical MAP-2 immunostaining in a focal ovine head impact model.

Dendritic pathology associated with traumatic brain injury may be identified by microtubule associated protein-2 (MAP-2) immunohistochemistry. The aim of this study was to examine the dendritic response in the cerebral cortical mantle in an ovine head impact model using MAP-2 immunostaining as a marker for dendritic injury. The loss of cortical MAP-2 immunoreactivity at 2 h was recorded and quantitated using a computerised image analysis system applied to standard coronal brain sections obtained from 10 impacted and 3 control sheep. Coup and contrecoup cortical contusions were present in 9 of 10 impacted brains examined 2 h after injury. MAP-2 immunoreactivity was lost in all areas of cortical contusion irrespective of site and in otherwise histologically normal cortex. MAP-2 immunostaining was lost in over 45% of the whole cortical area (range 32-54%) and only 2% (range 0-5.5%) was associated with contusions. This study has shown that there is widespread loss of MAP-2 immunostaining following head impact in the cerebral cortical mantle (up to 54%) suggestive of early dendritic injury.

Cerebrovascular pressure transmission analysis as a guide to the pathophysiology of raised intracranial pressure.

1. Raised intracranial pressure (ICP) is a major factor associated with morbidity and mortality in patients with severe head injury. Identifying the mechanisms responsible for raised ICP may be difficult and, as a result, treatment prescribed may be non-specific and often ineffective. 2. Research aimed at obtaining more information from measurement of ICP was initially focused on measurements of compliance. This was achieved by introducing fluid volume into the craniospinal compartment and measuring the response. Although shown to be clinically useful, associated technical problems have precluded the routine use of these measurements. 3. Cerebrovascular pressure transmission (CVPT) analysis has been suggested as an alternative method of deriving more information from the ICP wave-form. Pressure transmission across the cerebrovascular bed is assessed by a systems analysis approach whereby blood pressure and ICP wave-form pairs are resolved by fast Fourier transform analysis into component harmonic frequencies, each with a specific amplitude and phase. These are expressed as a ratio or 'transfer function' for each harmonic peak. 4. Laboratory models have identified specific CVPT patterns associated with various causes of raised ICP. These studies have been extended to clinical practice and have been used to define patterns of CVPT in head-injured patients, which may be used to identify mechanisms responsible for raised ICP, thus assisting in directing treatment strategy. Clinical usefulness of this technique in patient management is currently under investigation.

Juvenile glaucoma linked to the GLC1A gene on chromosome 1q in a Panamanian family.

PURPOSE: To characterize clinically and genetically autosomal dominant juvenile-onset primary open-angle glaucoma in a Panamanian family. METHODS: Twenty members of a six-generation family underwent ophthalmologic examination and genetic screening with markers near the GLC1A gene on chromosome 1q. RESULTS: Linkage analysis disclosed evidence linking primary open-angle glaucoma in this family to the GLC1A gene on chromosome 1q, with a maximum lod score of 3.75 for marker D1S431 at an estimated recombination fraction of 0.00. CONCLUSIONS: This is the first report of a Panamanian family in which primary open-angle glaucoma is linked to the GLC1A gene on chromosome 1q.

Progress in head injury management.

Preventable secondary injury remains disturbingly common and can only be reduced by highly organized and integrated services, and careful and continuous monitoring. Continuous non- or relatively non-invasive bedside monitoring of factors closely related to brain metabolism and function is becoming a practical reality. To the extent that the complex changes initiated by traumatic brain injury are 'processes' rather than 'events' it may become possible for components of injury to be halted or reversed. Pharmacological therapy given early after injury may be able to reduce the harmful events initiated by the injury. Head injury management is multidisciplinary. Improvements in head injury outcome have come about through better organisation of services - efficient retrieval, early investigation and removal of clots, and management in experienced intensive care units. Australian neurosurgeons have played a leading role in defining standards of care, in organizing services and in raising public health issues related to head injury. With the increasing and necessary involvement of other specialists and the greater dependence on technically demanding intensive monitoring and medical management, it is important that neurosurgeons remain at the forefront of the care of patients with head injury and not simply be reduced to managing the surgical complications on request.(86).

The effect of bleaching agent on composite/enamel bonding.

This in vitro study evaluates the effect of an in-office light-activated hydrogen peroxide bleaching agent on the shear bond strength of composite resin to etched enamel. Specimens were divided into 4 groups. Group 1 specimens were not bleached and served as the control; Group 2 consisted of specimens bonded immediately after bleaching; Groups 3 and 4 of specimens bonded 1 and 2 weeks respectively after bleaching. The mean shear bond strengths (MPa) of Groups 2 (14.2 +/- 4.9), 3(19.2 +/- 3.2) and 4 (23.1 +/- 3.7) were lower than the value obtained in Group 1 (25.1 +/- 3.7). Groups 2 and 3 had significantly lower shear bond strengths than the unbleached Group 1 (25.1 +/- 3.7). It is suggested that bonding procedures be postponed for two weeks after any bleaching procedure had been done.

A head impact model of early axonal injury in the sheep.

Axonal injury (AI), one of the principal determinants of clinical outcome after head injury, may evolve over several hours after injury, raising the future possibility of therapeutic intervention during this period. A new head impact model of AI in sheep was developed to examine pathological and physiological changes in the brain resulting from a graded traumatic insult. In this preliminary study 10 anesthetized and ventilated Merino ewes were used. Head injury was produced by impact from a humane stunner to the temporal region of an unrestrained head. Eight sheep were studied for 1, 2, 4, or 6 h after impact. Two sham animals (no impact, 6 h survival) were also examined. Arterial blood pressure, intracranial pressure, and cerebral blood flow were monitored continuously. A physiological index of injury severity was calculated by weighting the percentage shift from preinjury values for each monitored parameter over the first hour after injury. Immunostaining with amyloid precursor protein (APP) was used as a marker of axonal damage and the distribution of APP positive axons was recorded according to a sector scoring method (APPS). Widespread AI was identified in 7 of the 8 impacted animals, around cerebral contusions and in hemispheric white matter, central gray matter, brain stem, and cerebellum, and was detected as early as 1 h after injury. The degree of axonal injury (APPS) correlated well with an index of physiological response to injury (r = 0.83, p = 0.005).

Cerebral oxygenation monitoring by near-infrared spectroscopy is not clinically useful in patients with severe closed-head injury: a comparison with jugular venous bulb oximetry.

OBJECTIVE: To compare continuous jugular venous bulb oximetry and cerebral near-infrared spectroscopy in patients with severe closed head injury. DESIGN: A prospective observational study. SETTING: Intensive care unit of a major teaching hospital. PATIENTS: Adults (n = 10) with severe closed-head injury (Glasgow Coma Scale score of < or = 8). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Jugular venous bulb oximetry, cerebral near-infrared spectroscopy, and cerebral perfusion pressure were measured continuously. A total of 3,691 paired measurements of near-infrared spectroscopy and jugular venous bulb oximetry were analyzed. Poor correlation (r2 = .04) between paired measurements and wide limits of agreement (-13% to +21%) were demonstrated. The mean difference between measurements was +/- 4% and the standard deviation of the mean difference was +/- 8.69%. The data were subsequently grouped according to three clinically significant subgroups of jugular venous bulb oxygen saturation reflecting low ( < 55%), normal (55% to 75%) and high ( > 75%) saturation values. Poor correlation and wide limits of agreement between the two methods of measurement were observed in all groups. Values recorded by near-infrared spectroscopy did not significantly change between the groups, and 14 clinically significant episodes of jugular venous bulb desaturation were not detected by near-infrared spectroscopy. CONCLUSIONS: Tissue oxygen saturation determined by near-infrared spectroscopy does not reflect significant changes in cerebral oxygenation detected by the global measurement of jugular venous bulb oximetry. This finding may be explained by inadequate signal detection and inaccuracies in the algorithm used to filter out extracranial components. Until these technical difficulties are addressed, near-infrared spectroscopy, as measured by the machine assessed in this study, cannot be routinely recommended for assessment of cerebral oxygenation in patients with acute head injury.

Juvenile glaucoma linked to GLCIA in a Panamanian family.

PURPOSE: To carry out clinical and genetic characterization of juvenile-onset primary open-angle glaucoma (POAG) inherited as an autosomal dominant trait in a Panamanian family. METHODS: Twenty-two members of a six-generation Panamanian family underwent an ophthalmologic evaluation. Blood samples were collected from 20 of these individuals for preparation of DNA for use in screening of microsatellite repeat genetic markers via polymerase chain reaction. RESULTS: Eleven living family members covering 4 generations were diagnosed as affected with open-angle glaucoma of primarily juvenile onset. Four of 6 other at-risk individuals examined and enrolled were characterized as unaffected and two as indeterminate. Two additional individuals were not included in this study because they were too young to characterize or to provide a blood sample. Three spouses of affected family members were also examined and found not to have glaucoma. Of clinical importance was the finding of markedly elevated intraocular pressure (IOP) in 2 affected brothers, both of whom were advised to have urgent filtration surgery; the finding of elevated IOP in the only seeing eye of the mother of these brothers, causing us to advise her to pursue more aggressive treatment; and the finding of early signs of glaucoma in a previously undiagnosed 9-year-old family member. Linkage analysis using selected microsatellite repeat markers in the 1q21-q31 region revealed strong evidence for linkage to the GLC1A gene with a maximum lod score of 3.75 for marker D1S431 at a recombination fraction of 0.00. CONCLUSIONS: The most likely interpretation of our data is that a mutation in the GLC1A gene is responsible for juvenile-onset POAG in this Panamanian family, thus expanding the countries of origin where this gene has been found to exist. The numbers of families with GLC1A glaucoma now reported from only a few centers worldwide raise questions about whether this disease may be more common than once thought. Evaluation of treatment histories and clinical outcomes in members of this and other previously reported families indicates that ophthalmologists need to understand the necessity for urgent filtration surgery in most cases of GLC1A glaucoma if vision is to be preserved.

Detection of cerebral venous desaturation by continuous jugular bulb oximetry following acute neurotrauma.

A prospective observational study was performed to assess the reliability of fibreoptic oximetric catheters and to identify the incidence and causes of jugular bulb oxygen desaturation in patients with acute closed head injury. There were twenty-five patients (30 +/- 16 years) with GCS < or = 8 in this study. Jugular bulb oximetry, mean arterial pressure, intracranial pressure, end-tidal CO2 and pulse oximetry were monitored continuously. Catheter calibration against a laboratory oximeter was performed post insertion and thereafter eight-hourly. Cerebral venous desaturation was defined as a jugular bulb oxygen saturation < 55% of > 10 minutes duration. There was a poor correlation for the first in vivo calibration (r2 = 0.602, P < 0.001, n = 25). Thereafter a close correlation between jugular bulb catheter and oximetry values was demonstrated (r2 = 0.868, P < 0.001, n = 205). Forty-two episodes of jugular bulb oxygen desaturation of 88 minutes mean duration (range 10 to 555) were observed. 83% occurred within 48 hours following injury. Hypocapnia was associated in 45% of episodes; hypoperfusion in 22%; raised ICP in 9% and a combination of the above in 24%. Validation with a laboratory oximeter is essential prior to continuous jugular bulb oximetry. Sustained episodes of cerebral venous desaturation are frequent within the first 48 hours following acute head injury. Factors such as hypocapnia and cerebral hypoperfusion that primarily reduce cerebral blood flow are predominant.

Rehabilitation and splinting of common upper extremity injuries in athletes.

Treatment of athletes and the injuries they sustain can be both challenging and rewarding. Each individual case requires a careful examination of the physical symptoms and the process leading up to the injury. From this, one attempts to determine the appropriate course of treatment aimed at minimizing lost time from sports and to develop preventive strategies to promote healing and prevent future injury. Open communication between the athlete and his or her physician, therapist, trainer, and coach facilitates the most innovative and effective treatment strategies, enabling the best possible result following an athletic injury to the upper extremity.

Medical management of the diabetic patient during podiatric surgery.

Diabetes mellitus commonly causes complications of the foot that can lead to surgery. The appropriate perioperative management of diabetic patients can reduce the morbidity and mortality associated with diabetic foot surgery and enhance wound healing. The authors review the effects of hyperglycemia, detail preoperative, intraoperative, and postoperative care, and describe anesthetic choices. An algorithm for management of hypoglycemia is offered.

Malignant fibrous histiocytoma: review and case report.

Malignant fibrous histiocytoma (MFH) is a rare tumour of the spermatic cord. We present the second reported case in Australia and review the literature, discussing the recommended management and prognosis of this condition.

Propranolol fails to lower the increased blood pressure caused by cold air exposure.

Cold air exposure stimulates a rise in mean arterial blood pressure (MAP) and plasma norepinephrine (NE). The specific contribution of the beta-adrenergic receptor to this pressor response is unknown. Therefore, we pretreated 12 normal men with placebo or a bradycardia-inducing amount of propranolol prior to exposing them to either 25 degrees C or 4 degrees C air. At 25 degrees C, propranolol pretreatment lowered heart rate (HR) and MAP. When we compared changes in MAP after their respective 30-min exposure at 25 degrees C and 4 degrees C, the cold elevated MAP by 18.4 +/- 1.5 mm Hg in subjects pretreated with propranolol compared with 13.0 +/- 2.5 mm Hg in subjects pretreated with placebo. Fingertip skin temperature (Tfing) measured at 4 degrees C, 9.5 +/- 0.8 degrees C in propranolol-pretreated subjects was lower than the 11.1 +/- 0.7 degrees C with that of placebo. Plasma NE increased equally during cold exposure with both placebo and propranolol pretreatment. We conclude that the beta receptor plays a minor role in generating the pressor response to cold air. Therefore, the effectiveness of acute administrations of propranolol for maintaining normotension in subjects exposed to cold environments may be attenuated.

Adrenergic responses to cognitive activity in a cold environment.

Adrenergic responses during physical stress such as cold exposure have been reported to differ from those responses observed during cognitive activity. Both the separate and the combined effects of cold and cognitive activity on catecholamine activity were examined in six male subjects. Alterations in plasma epinephrine and norepinephrine showed different patterns as a function of exposure to a 4 degrees C cold environment, a cognitive performance assessment battery (PAB), and the two conditions combined. Plasma epinephrine was not altered by exposure to cold and only slightly increased by PAB performance when given at 23 degrees C. However, epinephrine was substantially elevated by exposure to combined cold and PAB. Heart rate changes paralleled observed changes in epinephrine. Norepinephrine release was predominantly increased by cold exposure and was not altered by PAB performance.