✓ Current therapy for dural sinus thrombosis consists of supportive measures, anticoagulation therapy, and in some cases intravenous infusion of a fibrinolytic agent. A patient with extensive dural sinus thrombosis was successfully treated with local urokinase infusion. The technique and rationale for this aggressive therapy are discussed.

The high‐affinity uptakes of [3H]serotonin, [3H]‐glutamate, and γ‐[3H]aminobutyric acid were studied using a myelin‐free crude synaptosomal fraction prepared from the spinal cords of normal dogs and spastic dogs following sham treatment or dorsal bilateral rhizotomy surgery. Compared to sham‐operated controls, rhizotomy surgery of normal dogs produced, after 1 week, a 30% reduction in the Vmax value of [3H]glutamate, but did not alter the uptake of γ‐[3H]aminobutyric acid. This treatment also produced a 60% decrease in the Vmax value of [3H]serotonin. Comparison of the effect of rhizotomy surgery on normal and spastic dogs revealed that the spastic group had 60% higher Vmax values for uptakes of [3H]glutamate and γ‐[3H]aminobutyric acid. Comparison of sham‐operated spastic dogs and rhizotomy‐treated spastic animals showed that there was a 25% decrease in the uptake of both amino acids in the rhizotomy‐treated spastic group. Overall, the data (a) support the hypothesis that glutamate is the neurotransmitter from some of the primary afferents, and (b) suggest that sprouting of interneuronal amino acid transmitter systems may occur in the spinal cords of spastic dogs.

A case of cervical chordoma diagnosed by fine needle aspiration (FNA) is presented. The cytologic criteria for differentiating chordoma from chondrosarcoma and metastatic adenocarcinoma, the main diagnostic problems, include the finding of physaliferous cells and the presence of bland nuclear features. Significantly, chordomas lack true signet-ring cells. FNA of these rare midline vertebral neoplasms, which produce pain and spinal cord compression, can greatly facilitate diagnosis and optimal treatment.

Abstract: The high‐affinity uptake of [3H]serotonin, [3H]glutamate, and [3H]‐γ‐aminobutyric acid (3H]GABA) and the Na+‐independent binding of [3H]glutamate and [3H]GABA were studied using spinal cord preparations obtained from normal mongrel dogs and from dogs made paraplegic by midthoracic spinal cord crush. Lumbosa‐cral regions of the spinal cord were removed either before (1 week) or after (3 to 8 weeks) onset of spasticity. A myelin‐free synaptosomal fraction was obtained by cen‐trifugation and used for studying high‐affinity uptake and for preparing synaptic plasma membranes for Na+‐inde‐pendent binding experiments. For the paraplegic groups, the uptake of 30 nM [3H]serotonin was 66 and 18% of control values after 1 and 3 weeks, respectively. Eadie‐Hofstee analysis of [3H]serotonin uptake showed a 90% reduction in Vmax for the paraplegic group relative to control values, thereby indicating the expected loss of descending serotonergic pathways. The high‐affinity uptakes of 1 μM [3H]glutamate and [3H]GABA were the same in both the control and nonspastic paraplegic groups after 1 week. However, after 3 weeks, the uptakes of [3H]glutamate and [3H]GABA were 60‐70% higher for the spastic group than for the control animals. For both amino acids, Eadie‐Hofstee plots revealed no difference in Km and higher Vmax for the spastic group relative to control values. After 1 and 3 weeks, the Na+ ‐independent binding of 5 nM [3H]glutamate was 40‐85% higher and the binding of 10 nM [3H]GABA was 40‐60% lower for the paraplegic groups relative to the values for the control animals. Scatchard analysis revealed significant changes in Bmax values for both amino acids. Overall, the data indicate an increase in segmental amino acid excitatory influence which occurred when signs of spasticity were evident.

The lack of an objective method for diagnosing thoracic outlet syndrome and monitoring the results of treatment has prevented a clear understanding of its natural history and the indications for surgery. Although one can detect vascular compression, the majority of patients have symptoms that are primarily neurogenic; and neither electromyograms nor studies of nerve conduction velocity has proved consistently helpful in their evaluation. We have studied evoked responses in 22 patients and believe that this technique allows selection of patients with significant neural compression for operative treatment. In this procedure, a bipolar stimulating electrode is placed on the median and ulnar nerves at the wrist; and bipolar recording is performed from active electrodes placed at Erb's point, over the spines of C6 and C2, and over the contralateral parietal scalp, all referenced to a midfrontal electrode. A minicomputer temporally summates the low-amplitude potentials elicited by repetitive electrical stimulation to increase the signal to noise ratio and therefore distinguish the potentials of interest from the background bioelectric activity. Normative values have been determined, allowing detection of changes in conduction of the electrical activity that occur between the sites of stimulation and the sites of recording. Of 19 new patients, 13 had abnormal evoked responses. Nine of these underwent surgical treatment; eight obtained good or excellent results. Abnormalities in evoked responses disappeared after operation in seven of the eight in whom it was measured. Four patients with abnormal responses but no surgery are being evaluated. Two of three long-term patients with recurrent symptoms had abnormal evoked responses that changed after treatment. Longer follow-up is needed to determine if this method is helpful in selecting patients for operative treatment or in monitoring its results.

The properties of carnitine transport were studied in rat brain slices. A rapid uptake system for carnitine was observed, with tissue-medium gradients of 38 +/- 3 for L-[14CH3]carnitine and 27 +/- 3 for D-[14CH3]carnitine after 180 min incubation at 37 degrees C in 0.64 mM substrate. Uptake of L- and D-carnitine showed saturability. The estimated values of Km for L- and D-carnitine were 2.85 mM and 10.0 mM, respectively; but values of Vmax (1 mumol/min/ml intracellular fluid) were the same for the two isomers. The transport system showed stereospecificity for L-carnitine. Carnitine uptake was inhibited by structurally related compounds with a four-carbon backbone containing a terminal carboxyl group. L-Carnitine uptake was competitively inhibited by gamma-butyrobetaine (Ki = 3.22 mM), acetylcarnitine (Ki = 6.36 mM), and gamma-aminobutyric acid (Ki = 0.63 mM). The data suggest that carnitine and gamma-aminobutyric acid interact at a common carrier site. Transport was not significantly reduced by choline or lysine. Carnitine uptake was inhibited by an N2 atmosphere, 2,4-dinitrophenol, carbonylcyanide-N-chlorophenylhydrazone, potassium cyanide, n-ethylmaleimide, and ouabain. Transport was abolished by low temperature (4 degrees C) and absence of glucose from the medium. Carnitine uptake was Na+-dependent, but did not require K4+ or Ca2+.

Twelve female mongrel dogs were made paraplegic by midthoracic spinal cord transection. Beginning at 9 weeks posttransection, either glycine (50 mg/kg) or saline was injected intramuscularly each day and the signs of spinal spasticity were assessed clinically. After treating the dogs for 3 weeks, we removed the lumbar enlargement of each dog and microdissected it into gray and white areas which we assayed for glycine, glutamate, and aspartate content. Some of the clinical signs of spasticity improved in the animals injected with glycine compared to the saline-injected controls. The content of glycine was significantly elevated in the central gray matter and ventral medial white matter of the glycinetreated dogs. The levels of glutamate were also significantly elevated in the central, lateral ventral, and medial ventral gray matter and in the dorsal lateral and ventral medial white matter of the glycine-treated dogs. The possible role of these segmental putative neurotransmitters in spinal spasticity is discussed.

Spasticity may result in part from segmental spinal disinhibition. We determined the content and specific activity of glycine (the putative neurotransmitter thought to mediate spinal postsynaptic inhibition) and serine (the probable precursor of glycine) in feline spastic spinal cord following the intra-aortic administration of two labelled precursors of glycine--14C-D-glucose and 14C-L-serine. The specific activities of both glycine and serine were significantly reduced in the ventromedial, central, and dorsal spinal gray matter in spastic animals. Glycine content remained at control values but serine content increased in spastic spinal cord. This study suggests that glycine turnover decreases in spasticity, owing to its diminished release, and supports neurophysiologic evidence of a decrement in postsynaptic inhibition.

The authors review treatment and results in 45 cases of medulloblastoma arising in childhood. The surgical mortality rate observed was 11%. Of those completing postoperative cerebrospinal irradiation at this institution, 53% have survived for 3 years, 41% for 5 years, and 22% for 10 years. The extent of surgical resection of the cerebellar tumor had no significant bearing on the prognosis. Those cases remaining free of recurrent disease had received significantly higher doses of postoperative irradiation, approaching 5000 rads to the whole brain or posterior fossa and 4000 rads to the spinal axis. Repeat irradiation and chemotherapy (vincristine, the nitrosoureas, and methotrexate) provided good palliation in most cases and significantly extended the survival time. However, 28 of 29 patients who developed locally recurrent or metastatic disease have died. Vincristine was considered the chemotherapeutic drug of choice and in 14 cases its use was associated with remissions lasting 2 to 18 months. The combination of chemotherapy and repeat irradiation was followed by remissions of longer duration compared to retreatment by irradiation alone when the disease recurred within 2 years. The inherent value of ventricular shunting procedures and steroid therapy for recurrent intracranial disease could not be ascertained. The findings in this study suggest that the primary treatment of medulloblastoma should be extended to include chemotherapy and optimum radiation therapy, since once recurrent disease develops retreatment is essentially palliative and a fatal outcome is virtuallly certain.

Twenty meningomyelocele patients with nonfunctional ventricular shunts or no shunts were studied radiologically. This group was compared to a second group of 4 patients with functional shunts. The various techniques are compared and discussed. Pantopaque ventriculography is a potentially dangerous procedure. Radioisotope ventriculography appears to be a safe and useful method of diagnosing syringohydromyelia. Ventricular decomposition by means of a shunt appears to be an effective treatment.

Kaolin-induced hydrosyringomyelia in dogs has been investigated by radioisotope ventriculography using both cerebrospinal fluid radioassay and scintigraphy. The hydromyelic central canal can be differentiated from the spinal subarachnoid space by scintigraphy, Serial studies show that hydromyelia arises rapidly to decompress the associated hydrocephalus in surviving animals. Syringomyelia, after a delayed onset, originates from the enlarged central canal. Radioisotope ventriculography may be a useful clinical aid in the diagnosis of hydrosyringomyelia.

Dogs were made paraplegic by complete mid-thoracic spinal cord transection. At one, three, eight, and twelve weeks post-transection the lumbar cord was removed and the dorsal grey matter microdissected from L2–3 and the content of ɤ-aminobutyric acid (GABA) determined. An initial decrease in GABA levels was followed by a gradual increase in content which correlated with the progressive development of spinal spasticity. By twelve weeks post-transection, GABA was elevated 68% above controls.

The catecholamine hypothesis of progressive spinal cord necrosis following mechanical trauma was investigated with the histofluorometric method. Forty-four adult mongrel dog were examined as control, L1 crush-injured, and crush-injured with prior T1 total transection groups. In crush injured dogs, catecholamines were present in a 1 cm length of white matter at the crush site, with the greatest accumulation in the deep lateral and ventral funiculi. Gray matter fluorescence was not enhanced. Prior transection did not abolish the intense accumulation of catecholamines at the site of the cord injury. We propose that the catecholamines accumulating at the cord injured site are not central in origin, but represent an uptake mechanism into white matter as a reflection of cord microperfusion.

Hight, Betty R.N.*; Redelman, Kathleen R.N., B.S.*; Hall, Peter V. M.D.* Author Information

Dogs were made paraplegic by complete mid-thoracic spinal cord transection. The content of glycine, glutamate, aspartate, and γ-aminobutyric acid were determined in ventral and central grey matter from the lumbar enlargement of the spinal cord at 1, 3 and 8 weeks after transection. A rapid decrease in the content of aspartate and glycine accompanied the onset of spasticity. By the eight week post-transection, aspartate and glycine had decreased to less than 50% of control levels.

Radioisotope ventriculography was applied clinically in myelodysplastic hydromyelia in three groups of patients: two patients with normal ventricles, two with obstructive hydrocephalus, and 16 with myelodysplasia. In the myelodysplastic group, radioassay in one patient demonstrated flow of radioistope down the hydromyelic cavity. Twenty scintigraphic studies on 16 myelodysplastic patients showed hydromyelia was present in all patients with spontaneously compensated hydrocephalus but in none of those with functional ventricular shunts. This relation between the hydromyelia and disordered ventricular hydrodynamics supports the Gardner hypothesis of myelodysplasia. Radioisotope ventriculography appears a safe and useful method of diagnosing hydrosyringomyelia and evaluating treatment by means of ventricular decompression.