Cervical disc rupture causing vertebrobasilar insufficiency.

A case of vertebrobasilar transient ischemia and posterior cerebral infarction caused by a ruptured cervical disc is reported. The causes of extrinsic vertebral artery compression are reviewed.

Cortical biopsy in Alzheimer's disease: diagnostic accuracy and neurochemical, neuropathological, and cognitive correlations. Intraventricular Bethanecol Study Group.

Neurochemical assessments were performed on biopsy samples taken from the right frontal lobe of patients diagnosed with Alzheimer's disease (AD), before the implantation of a ventricular catheter and pump assembly for the infusion of bethanechol chloride as an experimental therapy. The pathologically diagnosed patients with AD (n = 35; mean age, 67 +/- 1.5 yr) were compared with a group of samples from normal age-equivalent autopsied controls (n = 22; mean age, 68 +/- 2 yr) and autopsied AD brains (n = 11; mean age, 73 +/- 2 yr). Samples were assayed for choline acetyltransferase (ChAT), acetylcholinesterase, binding to [3H]quinuclidinyl benzilate as an index of total muscarinic cholinergic binding, and [3H]pirenzepine binding as an index of M1 cholinergic receptor subtype binding. Mean levels of ChAT activity were decreased in the biopsied patients to 36% of age-matched autopsied controls. The loss of ChAT activity correlated significantly with the Mini-Mental State Examination, an index of global cognitive function. Mean ChAT activity in autopsied AD cortex was further decreased compared with controls, indicating continuous decline through the course of the disease. Acetylcholinesterase followed a similar, less dramatic decline. No differences were found in [3H]quinuclidinyl benzilate binding or [3H]pirenzepine binding between biopsied and autopsied controls. Neuritic plaque counts did not correlate with either the Mini-Mental State Examination or ChAT activity in the biopsy specimens.(ABSTRACT TRUNCATED AT 250 WORDS)

Intracerebroventricular bethanechol chloride infusion in Alzheimer's disease. Results of a collaborative double-blind study.

The use of intracerebroventricular bethanechol chloride infusion in patients with Alzheimer's disease was first reported in 1984. An initial trial in four patients demonstrated the feasibility of this approach for cholinergic drug delivery to the brain, but objective improvement in cognitive function was not documented. A collaborative placebo-controlled double-blind crossover study has now been carried out in 49 patients with biopsy-documented Alzheimer's disease. The results demonstrate a statistical improvement in Mini-Mental State scores and significantly slower performance on Trails A testing during drug infusion. Other neuropsychological test scores were not similarly affected. The degree of improvement was not sufficient to justify further treatment of Alzheimer's disease patients by intracerebroventricular infusion of bethanechol chloride. The drug delivery system used in the study was well tolerated, with two irreversible complications in more than 50,000 patient days.

Anterior cervical discectomy with hydroxylapatite fusion.

The outcome of microscopic anterior cervical discectomy with iliac crest interbody fusion in a group of 75 patients was compared with that of microscopic anterior cervical discectomy with synthetic hydroxylapatite fusion in a group of 84 patients. The rate of relief of myelopathy (70%) was similar in both groups, but those who underwent synthetic fusion had better long-term relief of radiculopathy, less need for a second operation at the same or an adjacent level, no resorption of the bone plug, comparable spinal alignment and stability, and the elimination of complications at the iliac crest donor site. The data suggest that hydroxylapatite fusion may be equal or superior to autologous iliac crest interbody fusion for anterior cervical disc surgery.

Revascularization of the extracranial vertebral artery at any level without cross-clamping.

Hemodynamic insufficiency resulting from extracranial vertebral artery stenosis or occlusion is believed to be the major cause of vertebrobasilar transient ischemic attacks. The major difficulties in treating this disorder have been exposure of the vertebral artery distal to the stenosis and the risk of vertebral artery cross-clamping for vein grafting or carotid artery transposition. The authors describe a new technique for vertebral artery reconstruction at any level by the use of an intraluminal shunt, thus avoiding the necessity to cross-clamp the artery. This procedure was successfully performed at all three levels of the extracranial vertebral artery: C7-4, C3-1, and C-1 to the foramen magnum. The technique of exposure of the vertebral artery at these three levels and the method of vein grafting without cross-clamping are described. The initial results of the procedure are presented.

Combined subclavian-external carotid and superficial temporal-middle cerebral artery bypass graft.

A variation of a superficial temporal-middle cerebral artery bypass is presented that can serve as a surgical alternative to long vein subclavian-middle cerebral artery grafting in patients with common carotid artery occlusion and symptoms of ipsilateral ischemia. A vein graft from the subclavian to the external carotid artery at the carotid bifurcation is performed simultaneously with a standard superficial temporal-middle cerebral artery bypass. Advantages of this procedure over a long subclavian-middle cerebral artery vein graft are the technical simplicity associated with a standard superficial temporal-middle cerebral artery bypass, higher patency rates, and lower risk of graft leakage or torsion. Three patients have undergone this procedure, and all had patent bypasses one year after operation.

Nontraumatic dissecting aneurysm of the vertebral artery. Case report.

A case is described of a nontraumatic dissecting aneurysm of the vertebral artery, which presented as a subarachnoid hemorrhage (SAH). Differentiation from vasospasm and from atherosclerosis is critical. Dissection between the adventitia and media should be noted in the differential diagnosis of SAH when an aneurysm or vascular malformation is not demonstrated angiographically.

Intracranial pressure in nontraumatic ischemic and hypoxic cerebral insults.

Intracranial pressure (ICP) and cerebral perfusion pressure were monitored in 12 patients who were comatose secondary to hypoxic (five cases) or hypotensive (seven cases) nontraumatic cerebral insults. Patients who were hypotensive but not hypoxic developed significant increased ICP. In patients who were comatose from hypoxic cerebral insults without hypotension, ICP was normal. When an increase in ICP was diagnosed, patients were managed aggressively so as to improve cerebral perfusion and lower ICP. Although a functional salvage rate of 25% was obtained, this may reflect the severity of the initial cerebral insult rather than the effect of treatment. In order to prevent the potential deleterious effects of raised ICP, it is concluded that monitoring ICP and maintaining adequate perfusion may be warranted in comatose patients who have suffered nontraumatic diffuse ischemic but not purely hypoxic cerebral insults.

Comparison of hydrogen clearance and 14C-antipyrine autoradiography in the measurement of spinal cord blood flow after severe impact injury.

Spinal cord blood flow was measured by two different techniques in normal and traumatized cat spinal cord. Flow was measured in the thoracic cord after severe (500-gm-cm) impact injury at T-6. Blood flow was measured sequentially at two sites for 7 hours after trauma using the hydrogen clearance technique, and spatially at many sites but at selected times by means of the 14C-antipyrine autoradiographic method. The two techniques gave similar results. Control white-matter blood flow in the lateral funiculus was 11.13 +/- 1.29 ml/min/100 gm in the hydrogen clearance series, and 11.07 +/- 3.16 gm blood/min/100 gmin the antipyrine series. Following injury, blood flow remained in the control range until 1 hour after trauma, when ischemia became the major pattern. From 4 to 8 hours following trauma, several categories of flow patterns emerged. In one group of animals, white-matter blood flow returned to control levels at some points along the length of cord surveyed, but remained depressed at adjacent cord levels. In another category of animals, most sites in the white matter had flows approaching control levels by 7 to 8 hours. In yet another group, all sites examined, although a limited number, showed ischemia. In contrast, gray-matter ischemia appeared earlier (25% of control levels at 1 hour), had a sharper focus, and persisted in the period examined. The differences in blood flow between gray and white matter and the longitudinal variation in white-matter flow suggested that the hydrogen clearance method should be verified by autoradiography for accuracy of spatial flow patterns.

Loss of autoregulation and posttraumatic ischemia following experimental spinal cord trauma.

Blood flow in the dorsolateral funiculus of the cat thoracic spinal cord was studied after severe experimental cord injury, using a modification of the hydrogen clearance technique. Autoregulation was intact during the initial 60 to 90 minutes after cord injury, but was then lost coincident with the onset of ischemia. The data suggest that the ischemic response to spinal cord injury is mediated both by the loss of autoregulation and by relative vasoconstriction of the resistance vessels. Therapeutic intervention aimed at maintaining perfusion during the early posttraumatic period may prove of value in reversing or limiting some elements of dysfunction due to the secondary injury of ischemia.

Alteration of posttraumatic ischemia in experimental spinal cord trauma by a central nervous system depressant.

Blood flow after severe experimental injury to the thoracic spinal cord was studied in cats, using a modification of the hydrogen clearance technique. Gamma hydroxybutyrate, a central nervous system depressant, was shown to markedly alter the ischemic response to injury if given during the early posttraumatic period. Other vasoactive drugs investigated had no effect on posttraumatic ischemia. Therapeutic intervention during the early posttraumatic period aimed at increasing blood flow while decreasing the metabolic requirements of the injured cord may prove of value in reversing or limiting some elements of long-tract dysfunction due to the secondary ischemic insult.

Altered blood flow and secondary injury in experimental spinal cord trauma.

A modification of the hydrogen clearance technique was used to study blood flow in the dorsolateral funiculus of traumatized thoracic spinal cord in cats. The result of this study show that ischemia occurred in all animals both at the level of trauma, and 1 cm below the site of trauma. There was, however, a period of over 1 hour after trauma during which blood flow was maintained at both sites. This investigation not only confirms the presence of ischemia in the lateral funiculus of the injured spinal cord but suggests that a period of time exists in the posttraumatic period during which pharmacological intervention may alter the ischemic response and possibly prevent secondary injury resulting from the ischemia.

Cerebral manifestations of ergotism. Report of a case and review of the literature.

A patient with diffuse and focal cerebral dysfunction was found to have absent peripheral pulses. Cerbral angiography revealed evidence of an arteritis with bilateral high grade carotid stenosis. When there was no laboratory confirmation of the arteritis, an iatrogenic etiology (ergotism) was suspected. This was later confirmed by the patient. The pertinent literature on ergotism is reviewed, and it is emphasized that ergotism may develop in patients on therapeutic doses of the drug.