William E. Hunt

Painful ophthalmoplegia: Its relation to indolent inflammation of the cavernous sinus

RETROORBITAL PAIN accompanied by ophthalmoplegia was first described by Charcot, who called it “ophthalmoplegic migraine.” This term has been loosely applied to a number of pathologically unrelated disorders that have slinilar clinical manifestations. Pain and ophthalmoplegia may be caused by [ l] aneurysm of the internal carotid artery at the posterior wmmunicating junction, [ 21 neoplasm, [ 31 carotid-cavernous fistula, [4] gummatous periostitis about the orbital fissure, or [5] meningovascular syphilis with oculomotor palsy. A dilated sclerotic carotid artery may cause these symptoms by pressure upon the third cranial nerve just prior to its entry into the cavernous sinus (we observed this in a patient with retroorbital p i n and oculomotor palsy who was explored in the erroneous belief that the lesion was a saccular aneurysm). After excluding these identifiable lesions, there remain a number of cases of more obscure etiology. Transitory third cranial nerve palsy probably occurs in some cases of paroxvsmal vascular headache of the migraine type. This may be due to dilation and edema of the cerebral arteries adjacent to the oculomotor nerve in the subarachnoid spnce.1 The diagnosis of “ophthalmoplegic migraine” should be reserved for these cases. This paper is intended to define a clinical entity, of somewhat obscure etiology, that cannot be termed “ophthalmoplegic migraine.” In the last seven years, we have observed 6 cases of retroorbital pain and involvement of the structures lying within the cavernous sinus and its wall. This syndrome is characterized by the following criteria: 11 Pnin may precede the ophthalmoplegia

Pediatric Neck Injuries

This review of pediatric neck injuries includes patients admitted to Childrens Hospital of Columbus, Ohio, during the period 1969 to 1979. The 122 patients with neck injuries constituted 1.4% of the total neurosurgical admissions during this time. Forty-eight patients had cervical strains; 74 had involvement of the spinal column; and 27 had neurological deficits. The injuries reached their peak incidence during the summer months, with motor-vehicle accidents accounting for 31%, diving injuries and falls from a height 20% each, football injuries 8%, other sports 11%, and miscellaneous 10%. There is a clear division of patients into a group aged 8 years or less with exclusively upper cervical injuries, and an older group with pancervical injuries. In the younger children, the injuries involved soft tissue (subluxation was seen more frequently than fracture), and tended to occur through subchondral growth plates, with a more reliable union than similar bone injuries. In the older children, the pattern and etiology of injury are the same as in adults. The entire cervical axis is at risk, and there is a tendency to fracture bone rather than cartilaginous structures.

Astrocytic Processes: A Route Between Vessels and Neurons Following Blood-Brain Barrier Injury

The fluorescent tracer Evans blue EB was studied after circulation time ranging from 30 seconds to 5 minutes following blood-brain barrier BBB injuries in 42 dogs. Selective neuronal stainings SNS, associated with BBB injuries, occurred to a high degree. This phenomenon was examined by modifica-tions in existing fluorescence techniques. The mechanism of SNS was seen to lie in an almost imperceptible transport of EB along astrocytic processes connecting SNS with the adjacent vasculaturc. This report presents visual evidence under pathological conditions, and supports the concept of astrocytic processes as the normal route of transport between blood vessels and neurons. This requires long exposure photomicrographs since the fluorescing material is subtle within the ncuroglial processes.

Ruptured Anterior Spinal Artery AneurysmRepair via a Posterior Approach

A case of aneurysm at the junction of the vertebrospinal and anterior spinal arteries at the level of C-1 is presented. There was severe intracranial subarachnoid hemorrhage with subsequent right hemiplegia and 6th nerve palsies. Angiograms showed an anomalous arrangement of the arteries, but no arteriovenous malformation was seen. The lesion was repaired via a posterior approach. Anatomical and technical considerations of this approach are discussed. A review of the pertinent literature is presented.

The Tolosa-Hunt syndrome: a problem in differential diagnosis.

The authors give a review on the Tolosa-Hunt Syndrome. They discuss its differential diagnosis, appropriate diagnostic and therapeutic measures for the evaluation of this painful ophthalmoplegia which may be combined with neurological deficit referrable to the anterior cavernous sinus.

Cerebral and spinal fluid anaerobism during circulatory arrest

RESTRICTION of canine cerebral circulation leads to an accumulation of tissue lactate proportional to time up to about ten minutes of total substrate deprivation.1 Following severe cerebral stress of almost any etiological category with or without obvious cerebral nutrient and oxygen deficiency, cerebrospinal fluid (CSF) lactate levels have been noted to be elevated., Following restoration of circulation after vascular interruption, CSF lactate levels are also increased.3 Both the rapidity of lactate egress from brain tissue to CSF and the absolute amount of lactate in CSF during acute ischemia are unknown. Since CSF lactate concentration may be a measure of “brain death,” knowledge of CSF lactate concentration with known cerebral tissue lactate (CTL) accumulation may be valuable during an extended and known period of circulatory deprivation. Also, such comparison may afford information regarding the mechanism and rapidity of the transfer of this important metabolite across the brain-CSF barrier. CSF has been considered representative of brain extracellular space for many constituent elements, and CSF lactate levels have been utilized to indicate cerebral metabolic pe r fo r rnan~e .~ ,~ This investigation casts doubt upon the validity of the CSF lactate content, during extended circulatory arrest, as being entirely representative of conditions existing within brain tissue. Also, relative rates of lactate accumulation in brain, CSF, and blood have been substantiated.

Blood and cerebrospinal fluid lactate during induced hypotension.

Abstract Cerebral anaerobism during induced arterial hypotension to mean arterial pressure (HOH) and trimethaphan infusion (TIH) was evaluated in 11 dogs by comparison of lactate in cerebrospinal fluid (CSF) and arterial blood. In six HOH dogs average normotensive control CSF and blood lactates were 1.79 (range 1.45–2.2) and 1.21 (range 0.7–1.8) mmoles/liter. At 5, 30, and 60 min posthypotension, average CSF and blood lactates were 1.93 (range 1.4–2.7), 2.33 (range 2.1–2.6), 3.16 (range 2.6–4.8) mmoles/liter and 2.35 (range 1.4–3.9), 6.30 (range 2.4–12.4), 8.54 (range 5.0–12.6) mmoles/liter, respectively. In five TIH dogs average control CSF and blood lactates were 1.74 (range 1.5–1.9) and 1.18 (range (0.32–2.10) mmoles/liter. At 5, 30, and 60 min posthypotension average CSF and blood lactates were 1.74 (range 1.4–2.1), 2.48 (range 1.6–3.5), 2.68 (range 1.9–3.7) and 1.56 (range 0.79–2.60), 3.76 (range 1.6–5.4), 4.16 (range 2.3–5.4) mmoles/liter respectively. Statistical analysis of CSF data shows that there is no significant difference between HOH and TIH lactate accumulation, and that 5–30 min are required for significant elevation over controls. Analysis of blood lactate shows significant elevation over controls during HOH by 5 min and during TIH by 30 min, with greater lactate accumulation in HOH than TIH by 60 min. Futility of using CSF lactate and advantage of employing blood lactate to monitor cerebral metabolism during hypotension is demonstrated.

Cerebral hemodynamic crisis. Physiology, pathophysiology, and approach to therapy.

The physiology and pathophysiology of the cerebral circulation have been discussed in relation to treatment of the cerebral hemodynamic crisis. Data are presented to show how cerebral vascular resistance, the intracranial compartments, and brain metabolic demand may be manipulated to effect internal decompression and raise local perfusion pressures. It is quite apparent that irreversibility occurs rapidly in cases of complete ischemia and therapeutic success is often limited by this fact. Application of sound therapeutic principles will limit the extent of cellular destruction. Of particular importance to the general surgeon treating the multiply injured patient, is the effect of anesthesia on intracranial pressure in patients with compromised intracranial volume reserve.

In vitro basilar and common carotid artery reactivity to alpha and beta stimulation.

INVESTIGATIONS INTO PROBLEMS of intracranial vascular physiology have been stimulated by a multiplicity of clinical difficulties encountered in cerebral vascular disease. One of these which has recently been found of great significance is arterial vasospasm. This is a vascular smooth muscle contraction of unusual magnitude and duration which is not reversed by known vasoactive substances. I t is essential to distinguish spasm from physiological vasoconstriction with mural tension changes readily influenced by a multitude of vasoactive substa1ices.l The consequences of vasospasm include brain infarction from decreased cerebral blood flow in the distribution of the spastic artery. The cause of spasm is not known but occurs in conjunction with subarachnoid hemorrhage, occlusive disease, and surgical manipulation.2 Also, although it is well known that large and small cerebral vessels react to numerous physiological environmental alterations, exact mechanisms are unknown. Prompted by the work of others3-7 on smaller cerebral vessels, the intrinsic myogenic properties of large vessels from dogs and monkeys in physiological environs were investigated in vitro. Thereby, extrinsic neural, autacoidal, and metabolic parameters which cannot be controlled adequately in vivo can be avoided. A large intracranial vessel, the basilar artery, was utilized, since in man this vessel is involved in vasospasm, angiographically and under direct observation,z.z as a result of primary disease processes.

Cerebral tissue lactate in trimethaphan-induced hypotension☆

Abstract Ischemic effects of profound sustained hypotension upon the brain utilizing trimethaphan have been investigated because of frequent clinical utilization by surgeons. In ten dogs hypotension (30 to 40 mm Hg MAP) was sustained for one hour. Cerebral tissue lactate accumulation was assessed at five, thirty, and sixty minutes. By thirty minutes lactate rose to four to five times control levels but this did not increase in extent by sixty minutes. During profound trimethaphan-induced hypotension the brain incurs a progressive and marked oxygen debt. After thirty minutes and up to one hour of sustained hypotension hypoxic levels of lactate are attained, possibly indicating irreversibility.