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Nerve transfers have been well described for the treatment of congenital and traumatic injuries in the brachial plexus and extremities. This series is the first to describe nerve transfers to reanimate the diaphragm in patients confined to long-term positive pressure ventilation because of high cervical spine injury. Patients who have sustained injury to the spinal cord at the C3 to C5 level suffer axonal loss in the phrenic nerve. They can neither propagate a nerve stimulus nor respond to implanted diaphragmatic pacing devices (electrophrenic respiration). Ten nerve transfers were performed in six patients who met these conditions. The procedures used end-to-end anastomoses from the fourth intercostal to the phrenic nerve approximately 5 cm above the diaphragm. A phrenic nerve pacemaker was implanted as part of the procedure and was placed distal to the anastomosis. Each week, the pacemaker was activated to test for diaphragmatic response. Once diaphragm movement was documented, diaphragmatic pacing was instituted. Eight of the 10 transfers have had more than 3 months to allow for axonal regeneration. Of these, all eight achieved successful diaphragmatic pacing (100 percent). The average interval from surgery to diaphragm response to electrical stimulation was 9 months. All patients were able to tolerate diaphragmatic pacing as an alternative to positive pressure ventilation, as judged by end tidal CO2 values, tidal volumes, and patient comfort. Intercostal to phrenic nerve transfer with diaphragmatic pacing is a viable means of liberating patients with high cervical spine injury from long-term mechanical ventilation.

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Although enlargement of pituitary adenomas during pregnancy is a well documented phenomenon, this is rarely seen with craniopharyngiomas. Discussed here is the case of a patient whose initial presentation, operation, rapid regrowth, and reoperation of a pathologically proven solid craniopharyngioma, occurred during the course of a single pregnancy. Further, the rapid regrowth of the tumor resulted in total blindness for 48 hours prior to reoperation. Repeat transsphenoidal operation resulted in a gross total removal, restoration of vision, and allowed for the cesarean section delivery of a healthy infant.

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L-Glutamate was microinjected into the nucleus tractus solitarii (NTS) in anesthetized (chloralose and urethane), paralyzed and artificially ventilated rats, and spinal cord blood flow (SCBF) was determined using a combination of labeled microspheres. Unilateral chemical stimulation of the NTS (n = 13) significantly decreased SCBF in the cervical cord from 43 +/- 6 (mean +/- SEM) to 28 +/- 4 (P < 0.05), in the thoracic cord from 35 +/- 3 to 24 +/- 4 (P < 0.01), and in the lumbar cord from 49 +/- 3 to 40 +/- 3 ml min-1 (100 g)-1 (P < 0.05). The decrease in SCBF was not due to the decrease in arterial blood pressure (ABP) because the SCBF during the chemical stimulation of the NTS was significantly smaller (P < 0.05) than the SCBF during controlled hemorrhagic hypotension (n = 11). Chemical stimulation of the NTS did not affect the reactivity of the spinal cord vessels to hypercapnia (n = 5). Microinjection of the vehicle solution into the NTS had no effects on spinal cord circulation (n = 9). These results suggest that the cell bodies within the NTS may play a role in the control of spinal cord circulation.

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The impact of human immunodeficiency virus (HIV) on the clinical presentations, causative organisms, and neurologic outcomes of patients with spinal infections is reviewed. Thirty-two patients with spinal epidural abscesses, vertebral osteomyelitis, or both were treated at an urban hospital over a 42-month period. Thirteen of these patients were confirmed by serologic analysis to be HIV seropositive. The diagnoses were confirmed by 30 open surgical procedures (14 anterior, 16 posterior) and seven percutaneous biopsies. Twenty-seven intraoperative cultures were positive and the remaining three patients had positive blood cultures prior to the surgical procedure. In both the HIV (+) and HIV (-) groups, Staphylococcus aureus predominated as the causative organism (overall rate: 72%). Mycobacterium tuberculosis was the second most common organism. The clinical presentations in both groups were similar with pain as the most frequent symptom and objective neurologic abnormalities on physical examination in 29 of the 32 patients (91%). The results of this analysis show that the clinical presentations and organisms cultured do not differ depending upon a concurrent HIV infection. Furthermore, the ultimate neurologic outcome of patients with spinal infections depends on their neurologic status at the time of treatment and not on their HIV status.

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Long-term positive pressure mechanical ventilation has been the standard of care for patients with respiratory insufficiency caused by high cervical spine injury. Stimulation of the phrenic nerves, and thus the diaphragm, with an implanted phrenic nerve pacemaker has provided adequate ventilation and an alternative to the standard. Diaphragmatic pacing, also known as electrophrenic respiration, requires an intact phrenic nerve to act as a conduit for the applied stimulus. Propagation of the stimulus is impossible if the injury sustained has led to axonal loss in the phrenic nerve. This may be expected if the damage to the spinal cord is at the C3-C5 level. If the cell bodies of the motor neurons in this region have been damaged, or direct injury to the phrenic nerve has occurred, then diaphragmatic pacing is not feasible by the traditional method. Microsurgical repair of peripheral nerves and nerve grafting have provided the impetus for research into anastomosis of a viable intercostal nerve to a nonfunctional phrenic nerve, with subsequent reinnervation of the diaphragm. Once successful axonal regeneration and diaphragmatic reinnervation have occurred, the distal phrenic nerve may then be paced. This case documents the first successful institution of electrophrenic respiration after intercostal to phrenic nerve anastomosis.

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N-Methyl-D-aspartic acid (NMDA) (10 pmol in 100 nl of 0.9% sodium chloride solution) was microinjected into the nucleus tractus solitarii (NTS) of urethane-anesthetized, paralyzed and artificially ventilated rats, and cerebral blood flow (CBF) was determined using a combination of labeled microspheres. Moderate hypertension within the upper limit of cerebral autoregulation was induced by blood transfusion in order to measure CBF at normotension. Arterial blood pressure (ABP) was decreased by unilateral microinjection into the NTS in these rats but remained within normotensive range. The CBF in the cerebral cortex ipsilateral to the stimulated NTS significantly (P < 0.01) decreased from 38 +/- 4 (mean +/- S.E.M) to 27 +/- 4 ml.min-1.(100 g)-1(n = 9). The cerebrovascular resistance (CVR) in the cerebral cortex ipsilateral to the stimulated NTS significantly (P < 0.01) increased from 2.6 +/- 0.3 to 4.1 +/- 0.7 mmHg per [ml.min-1.(100 g)-1]. Blockade of NMDA receptors in the NTS with D,L-2-amino-5-phosphonovalerate (AP5, 500 pmol) abolished the CBF decrease and CVR increase responses elicited by microinjection of NMDA into the NTS (n = 9). Blockade of non-NMDA receptors in the NTS with 6,7-dinitro-quinoxaline-2,3-dione (DNQX, 100 pmol) had little effect on the CBF decrease and CVR increase responses elicited by microinjection of NMDA into the NTS (n = 10). Microinjection of the vehicle solution into the NTS had no effects on cerebral circulation (n = 7). Cerebral autoregulation was well maintained at moderate hypertension induced by blood transfusion and at normotension returned from moderate hypertension following controlled hemorrhage (n = 8). These results suggest that the NMDA receptors in the NTS may be involved in the control of cerebral circulation.

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It was investigated that the cerebral blood flow (CBF) decrease response elicited by chemical stimulation of the caudal ventrolateral medullary depressor area (VLDA) is mediated via the rostral ventrolateral medullary pressor area (VLPA) and the cervical sympathetic nerve. The CBF was determined by radiolabeled microsphere technique in urethane (1.1-1.5 g.kg-1, i.p.) anesthetized Wistar rats. (i) Microinjection of L-glutamate (1.7 nmol) into the VLDA produced a significant (P < 0.01) decrease in CBF from 64 +/- 9 (mean +/- SEM) to 48 +/- 9 ml.min-1.(100 g)-1 and a significant (P < 0.01) increase in cerebrovascular resistance (CVR) from 1.7 +/- 0.2 to 2.4 +/- 0.4 mmHg per [ml.min-1.(100 g)-1] in the cerebral cortex ipsilateral to the stimulated VLDA side (n = 9). (ii) After cervical sympathectomy, L-glutamate was unilaterally microinjected into the VLDA. The CBF and CVR did not change significantly (n = 10). (iii) After depression of the VLPA neurons with muscimol (GABA agonist), L-glutamate was unilaterally microinjected into the VLDA. The CBF and CVR did not change significantly (n = 14). These results suggest that the pathway from the VLDA to control cerebral vessels may be mediated via the VLPA and the cervical sympathetic nerves.

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The cerebral blood flow (CBF) was determined by radiolabeled microsphere technique in urethane (1.1-1.5 g.kg-1, i.p.) anesthetized Wistar rats. Microinjection of L-glutamate (1.7 nmol) into the ventrolateral medullary depressor area (VLDA) produced a significant (P < 0.01) decrease in CBF from 64 +/- 9 (mean +/- S.E.M.) to 48 +/- 9 ml.min-1.(100g)-1 and a significant (P < 0.01) increase in cerebrovascular resistance (CVR) from 1.7 +/- 0.2 to 2.4 +/- 0.4 mmHg per [ml.min-1.(100g)-1] in the cerebral cortex ipsilateral to the stimulated VLDA side but not in other structures such as brain stem and cerebellum (n = 9). Cervical sympathectomy blocked the decrease in CBF and increase in CVR elicited by chemical stimulation of the VLDA (n = 10). Depression of the ventrolateral medullary pressor area (VLPA) neurons induced by microinjection of muscimol into the VLPA blocked the CBF decrease and CVR increase following chemical stimulation of the VLDA (n = 11). Microinjection of the vehicle solution into the VLDA had no effects on systemic and cerebral circulation (n = 7). These results suggest that a vasoconstrictor pathway to control cerebral vessels involves an excitatory projection from the VLDA to the VLPA and the changes in cerebral circulation are mediated by the cervical sympathetic nerves.

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Acute brain swelling is well known to be acute vasodilatation of cerebral vessels and sometimes results from brain injury. One of the causes of acute brain swelling may be disturbance of central control mechanisms of cerebral vessels. However, the presence of acute spinal cord swelling is little noticed. We present here a possibility that acute spinal cord swelling may be occur following the dysfunction of the cardiovascular center of the medulla. In urethane-anesthetized, paralyzed and artificially ventilated rats, the neurons in the rostral ventrolateral pressor area (VLPA), origin of the sympathetic nerve activities in the brain stem, were chemically stimulated by microinjection of L-glutamate and the spinal cord blood flow (SCBF) was determined using labeled microspheres. The SCBFs of cervical, thoracic, and lumbar cord decreased significantly from 27 +/- 3 (mean +/- S.E.M.) to 20 +/- 2 (p < 0.01), from 22 +/- 1 to 17 +/- 2 (p < 0.05), and from 41 +/- 5 to 26 +/- 3 (p < 0.05) ml.min-1.(100 g)-1, respectively (n = 12). The spinal cord vascular resistances (SCVRs) of cervical, thoracic, and lumbar cord increased significantly from 3.7 +/- 0.4 to 5.0 +/- 0.6 (p < 0.05), from 4.2 +/- 0.2 to 5.9 +/- 0.7 (p < 0.05), and from 2.5 +/- 0.2 to 3.8 +/- 0.4 (p < 0.05) mmHg per [ml.min-1.(100 g)-1], respectively (n = 12). These results suggest that the neurons within the VLPA may play a role in the control of spinal cord circulation. There is a possibility that the dysfunction of the VLPA may cause acute spinal cord swelling.

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Acute brain swelling is reported to be due to acute vasodilatation of cerebral vessels. One of the causes of acute brain swelling may be disturbance of central control mechanisms of cerebral vessels. It has been reported that the anatomical location of the area which controls cerebral circulation is related to the area which controls systemic circulation. However, the role of the cardiovascular center on cerebral circulation has not been clear. The present study was, therefore, undertaken to examine the effects of chemical stimulation of the medullary cardiovascular center [nucleus tractus solitarius (NTS), ventrolateral depressor area (VLDA), and ventrolateral pressor area (VLPA)] on cerebral circulation. In anesthetized, paralyzed and artificially ventilated rats, the neurons in the NTS, VLDA, and VLPA were chemically stimulated and the cerebral blood flow (CBF) was determined using labeled microspheres. The CBF decreased significantly and the cerebrovascular resistance (CVR) increased significantly by chemical stimulation of the NTS, VLDA, and VLPA. These results suggest that the neurons within the NTS, VLDA, and VLPA control cerebral vessels vasoconstrictively. There is a possibility that the dysfunction of the NTS, VLDA, and VLPA may cause acute brain swelling.

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Classical treatment of compound depressed skull fractures includes debridement and closure of all scalp wounds to minimize the risk of delayed intracranial infection. In selected situations, a nonsurgical approach may prove to be equally safe. Over a 33-month period, we evaluated 1075 patients for head trauma. There were 63 patients with non-missile, compound depressed skull fractures (9 of these 63 patients have been excluded for deaths that occurred within 4 days of admission). Patients with significant intracranial hematomas or dural violations over the convexity of the brain underwent formal surgical therapy. Surgical therapy was performed on 28 patients (52%; age 33 +/- 3 years; ISS 24 +/- 2) and it consisted of craniotomy with debridement, elevation of depressed fragments, repair of dural tears, and evacuation of hematomas. Nonsurgical treatment was used if there was no evidence of violation of the dura mater and of significant intracranial hematoma. If the following criteria were satisfied, then the nonsurgical approach was employed: no evidence of exposed brain or a cerebrospinal fluid leak, no pneumocephalus related to the fracture, no depressed fragments of bone more than 1 cm below the inner table of the skull, and no gross wound contamination. Nonsurgical therapy was used on 26 patients (48%; age 34 +/- 3 years; ISS 19 +/- 2) and it consisted of wound irrigation, debridement, and closure. In all 54 patients of both subsets of patients, intravenous antibiotics were administered for 5 to 7 days. After two additional days of observation, off antibiotics, the patients were discharged. There were no infectious complications related to the central nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)

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The object of this study was to investigate the role of the ventrolateral medullary pressor area in mediating the cardiovascular responses to experimentally induced global cerebral ischemia, and to test if excitatory amino acids or acetylcholine are the transmitters released in this brain region during these responses. The cerebral ischemic response was elicited in pentobarbital-anesthetized, artificially ventilated male Wistar rats by bilateral ligation of vertebral arteries followed by temporary clamping of the common carotid arteries. The pressor area was identified by microinjections of L-glutamate. Inhibition of neurons in this area by microinjections of muscimol, a gamma-aminobutyric acid receptor agonist, abolished the ischemic response, which demonstrated that this area is important in mediating these responses. Microinjections of a broad-spectrum excitatory amino acid receptor blocker (kynurenate), of specific antagonists for N-methyl-D-aspartic acid (NMDA) and non-NMDA receptors (injected alone or in combination), and of atropine failed to block the ischemic responses. These results indicate that: 1) the ventrolateral medullary pressor area mediates pressor responses to cerebral ischemia, and 2) excitatory amino acids or acetylcholine in this area do not mediate the cardiovascular responses to cerebral ischemia.

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The management of acute cervical spine injuries has traditionally used bed-based skeletal traction until all non-neurologic injuries have been evaluated. This treatment method substantially hinders the ability to transport patients and to perform imaging studies and surgical procedures. In contrast, early application of a halo/vest apparatus provides immediate cervical stabilization and facilitates the diagnostic work-up and treatment of the patients with multiple injuries. The records of all 78 patients admitted from February 1988 through June 1991 who had acute cervical spine fractures, subluxations, or both with a risk of instability were reviewed. All patients were treated with halo/vests and no patient deteriorated neurologically following halo/vest application. Twenty-nine patients (37%) had a total of 55 associated injuries including long bone/pelvic fractures in 17, thoracic injuries in 13, closed head injuries in 11, facial fractures in 6, noncontiguous spinal fractures in 5, and abdominal injuries in 3. The mean injury Severity Score (ISS) was 18 (range, 9-54). While in the halo/vest, 43 patients (55%) had a total of 99 diagnostic studies completed and 46 patients (59%) had a total of 76 surgical procedures performed. There were 35 neurosurgical procedures on 32 patients and 41 non-neurosurgical surgical procedures on 24 patients. Over the past year, 20 of 21 patients (95%) had their halo/vest placed in the emergency department. The data demonstrate that many diagnostic and surgical procedures need to be performed on patients with unstable cervical spine injuries.(ABSTRACT TRUNCATED AT 250 WORDS)

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In urethane-anesthetized, paralyzed and artificially ventilated rats, the neurons in the rostral ventrolateral medullary pressore area (VLPA) were chemically stimulated by microinjections of L-glutamate (1.7-5.0 nmol in 100 nl of 0.9% sodium chloride solution) and the spinal cord blood flow (SCBF) was determined using a combination of labeled microspheres (57Co, 113Sn and 46Sc). In order to measure SCBF at normotension, moderate hypotension within the lower limit of spinal cord autoregulation was induced by controlled hemorrhage (n = 12). Unilateral chemical stimulation of the VLPA in these rats increased arterial blood pressure (ABP) but it remained within normotensive range. The SCBFs of cervical, thoracic and lumbar cord decreased significantly from 27 +/- 3 (mean +/- S.E.M.) to 20 +/- 2 (P less than 0.01), from 22 +/- 1 to 17 +/- 2 (P less than 0.05), and from 41 +/- 5 to 26 +/- 3 (P less than 0.05) ml.min-1.(100 g)-1, respectively. The spinal cord vascular resistances (SCVRs) of cervical, thoracic and lumbar cord increased significantly from 3.7 +/- 0.4 to 5.0 +/- 0.6 (P less than 0.05), from 4.2 +/- 0.2 to 5.9 +/- 0.7 (P less than 0.05), and from 2.5 +/- 0.2 to 3.8 +/- 0.4 (P less than 0.05) mmHg per [ml.min-1.(100 g)-1], respectively. During the chemical stimulation of the VLPA, SCBF increased in response to the changes in arterial PaCO2 indicating that the reactivity of spinal cord vasculature was intact (n = 5).(ABSTRACT TRUNCATED AT 250 WORDS)

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This retrospective review permits limited conclusions due to the small sample size and the limited control of variables. The temporary prepump, percutaneous epidural catheter trial is a useful component of our protocol. This period provides important information relative to possible side effects and efficacy of pain. The trial does give an estimation for the starting point of the intrathecal dosage but, as we have demonstrated, this is, at times, at a greater dosage than previously had been predicted. We feel that this retrospective review supports the continued use of a prepump trial of epidural morphine prior to permanent intrathecal pump implantation.

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In urethane-anesthetized, paralyzed and artificially ventilated rats, the neurons in the rostral ventrolateral medullary pressor area (VLPA) were chemically stimulated by microinjections of L-glutamate (1.7-5.0 nmole in 100 nl of 0.9% sodium chloride solution) and the cerebral blood flow (CBF) was determined using a combination of labeled microspheres (57Co, 113Sn and 46Sc). In one group of rats (n = 11), unilateral chemical stimulation of the VLPA produced a significant (P less than 0.01) increase in arterial blood pressure (ABP), a significant (P less than 0.05) decrease in CBF, and a significant (P less than 0.01) increase in cerebrovascular resistance (CVR) in the cerebral cortex ipsilateral to the stimulated VLPA. The CBF was 52 +/- 3 (mean +/- S.E.M.) and 48 +/- 4 ml.min-1.(100 g)-1 before and during the chemical stimulation of VLPA; the CVR was 1.9 +/- 0.1 and 2.6 +/- 0.3 mmHg per ml.min-1.(100 g)-1 before and during the stimulation. In order to measure CBF at normotension, moderate hypotension was induced by controlled hemorrhage in another group of rats (n = 8). Unilateral chemical stimulation of the VLPA in these rats increased ABP but it remained within normotensive range. The CBFs of ipsilateral and contralateral cerebral cortices decreased significantly (P less than 0.05) from 57 +/- 14 to 41 +/- 9 and from 50 +/- 12 to 39 +/- 9 ml.min-1.(100 g)-1, respectively. The CVRs of ipsilateral and contralateral cortices increased significantly (P less than 0.05) from 2.6 +/- 0.6 to 3.5 +/- 0.8 and from 2.7 +/- 0.5 to 3.5 +/- 0.8 mmHg/[ml.min-1.(100 g)-1], respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

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In anesthetized (chloralose and urethane), paralyzed and artificially ventilated rats, the neurons in the ventrolateral medullary depressor area (VLDA) were chemically stimulated by microinjections of L-glutamate (2.5-5 nmole in 100 nl of 0.9% sodium chloride solution) and the cerebral blood flow (CBF) was determined using a combination of labeled microspheres (57Co, 113Sn and 46Sc). Unilateral chemical stimulation of the VLDA (n = 11) produced a significant (P less than 0.05) decrease in CBF of the cerebral cortex ipsilateral to the stimulated VLDA; the CBF was 41 +/- 5 (mean +/- S.E.M.) and 29 +/- 4 ml.min-1.(100 g)-1 before and during the chemical stimulation of VLDA. The decrease in CBF was not due to the decrease in arterial blood pressure (ABP) caused by the chemical stimulation of the VLDA because the CBF during the chemical stimulation of the VLDA was significantly smaller (P less than 0.01) than the CBF during controlled hemorrhagic hypotension (n = 10). In another group of rats (n = 6), moderate hypertension was induced by blood transfusion. Unilateral chemical stimulation of the VLDA in these rats decreased ABP but it remained within normotensive range. A significant (P less than 0.05) decrease in CBF (from 46 +/- 12 to 29 +/- 7 ml.min-1.(100 g)-1) and a significant (P less than 0.01) increase in cerebrovascular resistance (from 2.7 +/- 0.4 to 4.3 +/- 0.6 mmHg per [ml.min-1.(100 g)-1]) was observed in the ipsilateral cerebral cortex of these rats. Chemical stimulation of the VLDA did not affect the reactivity of the cerebral vessels to hypercapnea (n = 5).(ABSTRACT TRUNCATED AT 250 WORDS)

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In anesthetized (chloralose and urethane), paralyzed and artificially ventilated rats, the neurons in the nucleus tractus solitarius (NTS) were chemically stimulated by microinjections of L-glutamate and the cerebral blood flow (CBF) was determined using a combination of labeled microspheres (either 57Co, 113Sn and 46Sc or 141Ce, 85Sr and 46Sc). Unilateral chemical stimulation of the NTS (n = 14) decreased CBF significantly in most brain areas. The decrease in CBF was not due to the decrease in arterial blood pressure (ABP) because the CBF of the whole cerebral cortex during the chemical stimulation of the NTS was significantly smaller (P less than 0.05) than the CBF during controlled hemorrhagic hypotension (n = 10). In another group of rats (n = 6), moderate hypertension was induced by blood transfusion. Unilateral chemical stimulation of the NTS in these rats decreased ABP but it remained within normotensive range. A significant (P less than 0.05) decrease in CBF (from 62 +/- 28 (mean +/- S.D.) to 48 +/- 23 ml.min-1.(100 g)-1) and increase in cerebrovascular resistance (from 1.9 +/- 1.2 to 2.6 +/- 1.2 mm Hg per [ml.min-1.(100 g)-1]) was observed in the whole cerebral cortex of these rats. Chemical stimulation of the NTS did not affect the reactivity of the cerebral vessels to hypercapnea (n = 5). These results suggest that the cell bodies within the NTS may play a role in the control of cerebral circulation.

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The pressor (VLPA) and the depressor (VLDA) areas in the ventrolateral medulla were identified with the microinjection of L-glutamate (1.77 nmol/site) in artificially ventilated urethane-anesthetized male Wistar rats. Bilateral microinjection of a stable substance P (SP) agonist [pGlu5, MePhe8, Sar9]-SP(5-11)], abbreviated as DiMe, into the VLPA (6-600 pmol/site) produced a dose-dependent increase in blood pressure (BP). The effects on heart rate (HR) were variable. Intravenous pretreatment with a ganglionic blocker chlorisondamine (3.0 mg/kg, i.v.), but not with a vasopressin antagonist, blocked these responses. Similar microinjection of DiMe (6-600 pmol/site) into the VLDA produced a dose-dependent decrease in HR but had no effect on BP levels. The DiMe-induced bradycardic response elicited from the VLDA was blocked by i.v. pretreatment with atropine methylbromide (0.5 mg/kg, i.v.). These findings indicate that there are SP receptors localized on sympathoexcitatory neurons in the VLPA and that SP may be an excitatory neurotransmitter in this area. In the VLDA, the SP receptors appear to be localized on a subpopulation of neurons that affect vagal, but not sympathetic, outflow to the heart.

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