Thomas J. Lovely

Improvement of cortical morphology in infantile hydrocephalic animals after ventriculoperitoneal shunt placement

As a sequel to our previous descriptions of the pathological changes induced by hydrocephalus in the infantile cerebral cortex, the study presented here has evaluated the effects of surgical decompression on cortical cytology and cytoarchitecture. Hydrocephalus was induced in 14 kittens by the intracisternal injection of kaolin at 4 to 11 days of age. Nine of these hydrocephalic animals received low-pressure ventriculoperitoneal shunts at 9 to 15 days after kaolin injection; these animals were monitored preoperatively and postoperatively by ultrasound and were killed at various postshunt intervals up to 30 days. Five normal or saline-injected animals served as age-matched controls. At the time of shunt placement, the ventricular index confirmed that all recipient animals had attained moderate or severe degrees of ventriculomegaly. Within 3 days after shunt placement, the size of the lateral ventricles had decreased to control levels and was accompanied by rapid and dramatic improvements in behavior and skull ossification. When the animals were killed, gross inspection revealed that about half of the animals exhibited mild to moderate ventriculomegaly, with cortical mantles 50 to 80% their normal thickness. Tissue from frontal (primary motor), parietal (association), and occipital (primary visual) cortical areas was processed for light microscopic analysis. Pyknotic or dark shrunken neurons, which are found typically in hydrocephalic brains, were observed only occasionally in the cortex of shunted animals. Gliosis and mild edema were prevalent, however, in the periventricular white matter. The laminae of the cerebral cortex could be identified in all shunted animals. In those animals with mild residual ventriculomegaly, the entire cortical mantle was somewhat compressed, as evidenced by an increased packing density of neurons. Furthermore, the somata of some neurons were disoriented. Overall, these results indicate that most of the morphological characteristics of the cerebral cortex are preserved after surgical decompression and suggest that ventriculoperitoneal shunts may prevent neuronal damage and/or promote neuronal repair.

Effects of Hydrocephalus and Surgical Decompression on Cortical Norepinephrine Levels in Neonatal Cats

Norepinephrine (NE) changes during hydrocephalus, and the effects of surgical decompression on these changes, were studied using a new model of neonatal hydrocephalus. Kittens 4 to 10 days old received intracisternal injections of a sterile solution of 25% kaolin. Control kittens were injected similarly with sterile injectable saline. Ultrasonography was used to follow the progression of ventriculomegaly and the initial effects of the shunts. A subgroup of hydrocephalic animals was shunted using a cerebrospinal fluid lumbar-peritoneal catheter. Hydrocephalic animals were killed at approximately 25 days of age (16-21 days after kaolin injection). Surgical decompression was performed at 12, 16, and 17 days after kaolin injection; these animals were killed 30 days after the shunts were inserted. Control animals were killed at 29 and 53 days of age, to correlate with the ages of the hydrocephalic and shunted animals, respectively. Cortical samples equivalent to Brodmanns areas 4, 22, and 17 were measured for NE using high-performance liquid chromatography. Hydrocephalus caused NE levels to decrease significantly in all cortical areas. These alterations followed a rostrocaudal gradient in severity, with mean reductions of 65.8, 83.9, and 95.8% in areas 4, 22, and 17, respectively. Partial recovery occurred in animals that received shunts 16 and 17 days after kaolin injection, such that NE reductions of 75.7, 56.2, and 81.6% were noted in areas 4, 22, and 17, respectively. Shunting at 12 days after kaolin injection produced complete recovery in areas 4 and 22, with only a 67.7% decrease in area 17. These results suggest that the projection fibers from the locus ceruleus are damaged by the direct effects of hydrocephalus. Axotomy or neuropraxia of these fibers could result in decreases in NE throughout the cerebral cortex. In addition, there appears to be a period of time during which surgical decompression will allow neuropraxic fibers to recover with partial restoration of NE levels. Earlier insertion of a shunt appears to allow for more recovery than later decompression.

Intraoperative mapping of the trigeminal nerve root: technique and application in the surgical management of facial pain.

A method for intraoperative topographic mapping of the trigeminal nerve root using electrophysiological methods is described. A series of 15 patients under general anesthesia during microvascular decompression and selective posterior fossa trigeminal rhizotomy was studied. This method was used to study the localization of fibers of individual subdivisions of the intradural portion of the trigeminal nerve and as a guide for performing physiologically controlled, selective, microsurgical trigeminal rhizotomy.

A technique for placing ventriculoperitoneal shunts in a neonatal model of hydrocephalus

Induction of hydrocephalus in a neonatal animal with subsequent surgical decompression is the most analogous situation to the clinical state of infantile hydrocephalus. Described in detail is a reliable method for the placement of pressure-dependent ventriculoperitoneal shunts in neonatal kittens with hydrocephalus. Successful decompression can be quantified using ultrasound. This model allows for observation of hydrocephalic changes that may persist or be corrected after shunting, be they morphological, behavioral or biochemical. In addition, potential pitfalls in performing the procedure and in postoperative care of the kittens are addressed.

Unilateral trismus in a patient with trigeminal neuralgia due to microvascular compression of the trigeminal motor root

To our knowledge, only one prior case of trismus due to vascular compression has been reported. This was caused by vertebrobasilar dolichoectasia associated with multiple cranial neuropathies and was not treated surgical1y.t We report a case of unilateral trismus associated with typical trigeminal neuralgia, refractory to medical therapy, alleviated by microvascular decompression. The relevant anatomy of the trigeminal nerve is discussed, along with the pathophysiology and differential diagnosis.