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At least 19 recordsLinked to original sources
PubMed1988

The central-peripheral transitional regions of cranial nerves. Trochlear and abducent nerves.

Unlike all other nerves containing somatic efferent fibres, the trochlear nerve emerges from the dorsal aspect of the brainstem. It generally emerges as a single trunk which resembles a dorsal rather than a ventral spinal nerve rootlet in terms of its size and of the morphology and position of the central tissue projection which it contains. The morphology of the central-peripheral transition of the trochlear nerve is therefore correlated with its dorsal location rather than with the nature of its constituent fibres. By contrast, abducent nerve rootlets emerge from the ventral aspect of the neuraxis, in line with other cranial and with spinal ventral nerve rootlets which also contain somatic efferent fibres. Its rootlets resemble the latter in terms of their size, being much smaller than those of dorsal rootlets or the trochlear nerve. They possess two distinct types of central-peripheral transitional zone: those of the rostral rootlets resemble zones of cervical ventral spinal rootlets. Many of these emerge through a circumscribed thickening of the astrocytic glia limitans. Caudal abducent rootlets emerge through a tongue-shaped glial elevation projecting above the level of the surrounding brainstem surface, resembling Type 1 oculomotor rootlets.

Abducens Nerve↗
PubMed1975

Delayed trochlear nerve palsy in a case of zoster oticus.

A 57-year-old man with herpes zoster oticus developed a delayed fourth nerve palsy followed by transient intermittent sixth nerve weakness. Trochlear nerve lesions occur rarely with zoster, particularly in the absence of zoster ophthalmicus. A knowledge of the wide range of motor manifestations and the chronicity of meningitis with zoster will afford earlier diagnosis without resort to arteriography.

Diagnosis, Differential↗
PubMed1988

Trochlear nerve meningioma in von Recklinghausen's disease.

A trochlear nerve meningioma in a patient with von Recklinghausen's disease is reported. The tumour appeared to have originated from the trochlear nerve itself, having no connection either with the neurinomas present in the adjacent regions, or with the tentorium. Histological examinations revealed that the tumour was a meningotheliomatous meningioma and the trochlear nerve fibres were placed in the periphery of the tumours. It was noteworthy that diplopia was not detected either before or after the resection of the trochlear nerve with the tumour.

Adult↗
PubMed1987

The trochlear nerve of amphibians and its relation to proprioceptive fibers: a qualitative and quantitative HRP study.

The cells of origin of the trochlear nerve of urodeles, anurans and gymnophionans were labelled with HRP in order to compare the location and morphology of trochlear motoneurons and to find evidence for sensory fibers in the trochlear nerve of amphibians. Trochlear motoneuron perikarya were found in a ventral tegmental position predominantly on the contralateral side, but an ipsilateral cell was present in some specimens of urodeles and anurans. About 19 motoneurons were labelled in Ambystoma, about 60 motoneurons in Xenopus, and a maximum of 7 cells in Ichthyophis. Decussation of trochlear nerve fibers showed only in Xenopus a highly variable pattern. In urodeles, selective filling of the trochlear nerve labelled in addition to trochlear motoneurons a caudo-medical tectal group of about 20 neurons of the nucleus of the mesencephalic root of the trigeminal nerve. Gymnophionans showed also labelled cells of the mesencephalic trigeminal root in the caudal midbrain close to the trochlear nerve root. In some frogs, a few cells of the mesencephalic trigeminal root were labelled in the caudal tectum and occasionally in the velum medullare anterius. Comparison of the numbers of trochlear nerve fibers with HRP-labelled motoneurons revealed in Xenopus a proportion of 1.2:1, but of 2.7:1 in Ambystoma. However, counting both labelled motoneurons and cells of the mesencephalic trigeminal root resulted in a trochlear nerve fiber to labelled neuron proportion of 1.3:1 in Ambystoma much like in Xenopus. The numbers of superior oblique muscle fibers and of trochlear nerve fibers, but not of HRP-labelled motoneurons, increased significantly with size in Xenopus laevis. We suggest that increased peripheral branching of individual fibers within the trochlear nerve with size rather than differentiation of additional motoneurons takes place in growing postmetamorphic Xenopus. In contrast to other vertebrates studied so far, the trochlear nerve is a mixed nerve in Ambystoma and perhaps in Ichthyophis. Whether this reflects a primitive or a derived condition is at present unclear.

Ambystoma↗
PubMed1990

[Isolated trochlear nerve paralysis following head trauma].

39 cases with isolated trochlear nerve palsies of traumatic origin have been analyzed retrospectively. 18 patients (46%) had had cerebral contusion, 15 (39%) cerebral concussion, and 6 patients (15%) a minor head trauma. 33 patients had unilateral trochlear nerve palsies and 6 (all of them with cerebral contusion) bilateral. The degree of the palsies did not correlate with the severity of the head trauma. Essential pathogenetic mechanisms were frontal or occipital blows. We emphasize a fact hitherto underestimated in the literature, that even a relatively mild head trauma (cerebral concussion or minor head trauma) can cause isolated trochlear nerve palsies. This was the case in 21 of our 39 patients (54%). Simple clinical examination techniques are described (Bielschowsky phenomenon, pencil test), which allow detection of trochlear nerve palsies in most cases.

Adolescent↗
PubMed1988

Cavernous portion of the trochlear nerve with special reference to its site of entrance.

In a study of 80 cavernous sinuses in 40 cadavers, the trochlear nerve entered the cavernous sinus in 87.5% of cases before the crossing, in 7.5% at the crossing and in 5.0% after the crossing of the free and the attached margins of the tentorium cerebelli. In 77.5% of specimens the trochlear nerve showed a marked bend with flattening at the site of its entrance into the cavernous sinus. The nerve ran between the superficial and deep layers of dura, partly between them, in the thickness of the deeper layer, or deep to the deep layer but adherent to it. These findings do not conform with the description of its course by other workers in the past. In 72.5% of specimens the size of the trochlear nerve was larger during its course in the cavernous sinuses but in 20.0% of specimens such an increase in thickness was noted even in the posterior cranial fossa. Only in one specimen was the trochlear nerve adherent to the ophthalmic division of the trigeminal nerve. Cases showing the trochlear nerve entering the cavernous sinus after the crossing of the two margins of tentorium cerebelli and the splitting and branching of the trochlear nerve in the cavernous sinus have not hitherto been reported.

Adult↗
PubMed1989

Bilateral trochlear nerve paresis in hydrocephalus.

Three patients with nonneoplastic hydrocephalus had bilateral paresis of the trochlear nerves. Associated signs, including paresis of upgaze, light-near dissociation of the pupils, and convergence-retraction nystagmus, suggested rostral involvement of the mesencephalon. Trochlear nerve paresis and accompanying signs improved after revision of ventricular shunts in two patients. Bilateral trochlear nerve paresis may be a localizing sign of involvement of the superior medullary velum (the anatomic site of trochlear nerve decussation) by a dilated sylvian aqueduct and/or downward pressure from an enlarged III ventricle.

Adolescent↗
PubMed1988

Trochlear nerve palsy following minor head trauma. A sign of structural disorder.

Trauma-induced superior oblique palsy usually results from contusion or avulsion of the trochlear nerve or from decompensation of a congenital trochlear nerve palsy. Severe craniocerebral trauma is often associated with the former mechanism, whereas more minor closed-head injuries can decompensate a congenital phoria. We report a patient who developed an isolated trochlear nerve palsy following minor head trauma. Investigation revealed an unsuspected tentorial vascular malformation that was compressing the trochlear nerve in its subarachnoid course. In the absence of other features (e.g., documentation of old head tilt, large vertical fusion amplitudes) that support decompensation of a congenital phoria, compressive lesions should be sought in cases of fourth cranial nerve palsies that follow minor head trauma.

Cranial Nerve Diseases↗
PubMed1985

Bilateral trochlear nerve palsies. A clinicoanatomic correlate.

A patient with bilateral trochlear nerve palsies is presented. Computed tomographic (CT) brain scan localized an anterior cerebellar vermis lesion compressing the area caudal to the inferior colliculi where the fourth nerves decussate and exit the dorsal brain stem. This lesion was probably responsible for the bilateral trochlear nerve dysfunction. Pertinent anatomy and pathologic involvement are discussed.

Adenocarcinoma↗
PubMed1992

Cryptic angioma in the trochlear nerve. Excision of the invaded portion and successful repair with an autologous graft: case report.

Cryptic angiomas, which are intrinsic to cranial nerves, are uncommon. Such lesions involving the trochlear nerve have not been previously described. The authors have therefore found it interesting to report a case fortuitously discovered in a patient with trigeminal neuralgia who underwent a fifth nerve microvascular decompression through the supracerebellar space. The angioma was not responsible for the neuralgia, but because of its potential risk of bleeding, the lesion was treated by resection of the trochlear nerve in its invaded portion. Then, the nerve was successfully repaired with an autograft harvested from the distal part of the sural nerve.

Aged↗
PubMedDate not supplied

MR imaging of primary trochlear nerve neoplasms.

We present the clinical, anatomic, and MR imaging findings in six patients with seven primary trochlear nerve neoplasms, as well as the MR and clinical criteria that serve to establish the diagnosis of these rare cranial nerve neoplasms. Three patients had a history of neurofibromatosis and five patients had clinical evidence of a trochlear nerve palsy. Six of seven neoplasms produced localized, fusiform enlargement of the proximal cisternal segments of the trochlear nerves. The lesions that were visible on noncontrast MR scans (T1-, T2-, and proton density-weighted) had signal intensities that were virtually identical to normal brain parenchyma. All lesions showed intense, homogeneous enhancement on contrast-enhanced scans. Contrast-enhanced imaging was necessary for the detection of five of seven lesions and greatly increased the value of the MR study in all six patients.

Adult↗
PubMed1978

Isolated trochlear nerve palsies in herpes zoster ophthalmicus.

The clinical course of six patients with isolated trochlear nerve palsy as the only ocular motor manifestation of herpes zoster ophthalmicus has been analyzed. Spontaneous recovery occurred in only three. Review of the literature does not clarify the mechanism of such palsies, which potentially may result from the following conditions: local orbital muscle inflammation and ischemia; contiguous intracavernous spread of inflammation from the trigeminal nerve; and a concurrent but independent motor neuropathy or ganglionitis.

Adrenal Cortex Hormones↗
PubMed1978

Development of the trochlear nerve: loss of axons during normal ontogen.

Development of the trochlear nerve from day 11 of incubation through hatching was studied in white Peking duck embryos. Counts of fibers from the electron micrograph montages indicate that initially there is an abundant collateral sprouting which roughly coincides with the time of neuromuscular contacts, suggesting some sort of interaction between the developing nerve and the periphery. The maximum number of trochlear cells and fibers is present on day 12. Average cell and fiber counts on this day are 2325 and 47,386 respectively. Assuming all cells send their axons into the nerve and that all cell bodies are present within the trochlear nucleus, the ration of cells to fibers is 1:20. Average cell and fiber counts at hatching are 1338 and 1506 respectively. Thus, losses of approximately half the trochlear cells and of 97% of the fibers occur during normal development. Degenerating cells and fibers are first observed on day 13. Degeneration involves both the myelinated and the unmyelinated axons. The actual number of degenerating fibers which were observed, however, was very small compared to the number of fibers lost during development; thus, it is suggested that, in the majority of cases, fiber loss is perhaps via retraction of axon collaterals. In general, cell death slightly precedes axon loss, which suggests that the direction of the degeneration is from cell body to the axon. A cell/fiber ratio of approximately 1:1 is first observed on day 18 and remains so thereafter. Indirect evidence is discussed, suggesting that at least some cells which die during normal devleopment had sent their axon into the nerve prior to their death. Whether these axons make meaningful connections with the muscle is uncertain.

Animals↗
PubMed1989

Traumatic trochlear nerve palsy diagnosed by magnetic resonance imaging: case report and review of the literature.

Although head trauma is the leading cause of acquired trochlear nerve dysfunction, it receives little attention in the neurosurgical literature. A case is reported of closed head injury that resulted in a right superior oblique palsy in association with incoordination on the left side. Diagnostic imaging revealed a normal cranial computed tomographic scan and a left dorsal midbrain lesion on magnetic resonance imaging scan. The relevant anatomy is reviewed, as well as the action of the superior oblique muscle, its agonists and antagonists, and the clinical manifestations of superior oblique dysfunction. This case is one of the few we are aware of in which a relatively isolated trochlear nerve palsy is the result of a lesion that can be documented by diagnostic imaging, and the first in which the imaging modality is magnetic resonance imaging scan.

Adult↗
PubMed1991

[A case of brainstem vascular malformation with isolated trochlear nerve palsy as the initial symptom].

We report a 46-year-old, non-hypertensive man who suddenly developed isolated right trochlear nerve palsy. His diplopia was most prominent in the left lower gaze, and partially alleviated by head tilt to the left or by anteflexion of the neck. His CT scans showed a small high density area consistent with a hemorrhage in the lateral side of the right mesencephalic tectum. His MRI (T2-weighted images) showed a lesion consisting of mixed high- and iso-intensity areas with linear low intensity areas. The margin of the lesion was irregular and nodular. Cerebral angiography (prolonged injection) showed small feeding arteries (or capillaries) in the late arterial phase and dilated draining veins in the venous phase. No tumor stain, early draining veins, or capillary brushes were present. We thought he had an angioma (vascular malformation). AVM seemed unlikely. Review of the literature revealed that trochlear nerve palsy caused by a mesencephalic angioma is extremely rare. MRI and cerebral angiography (prolonged injection) seemed useful for the diagnosis of angiomas (Vascular malformations).

Brain Neoplasms↗
PubMed1979

Changes in axonal numbers in developing human trochlear nerve.

Complete axonal counts have been made in the intracranial parts of trochlear nerves from human fetuses of 9.2, 10 and 24 cm crown-rump length. A count was also made in the intraorbital part of the nerve from the 10 cm specimen. Schwann cell nuclei were also counted in typical cross sections, but do not necessarily reflect very accurately the schwann cell contents of the nerves. Axonal numbers conform to the propositions (1) that they do not all grow out at once, (2) do not all survive and (3) that degeneration may occur before or after myelination has begun. It seems inevitable that some loss of Schwann cells occurs in relation to the degeneration of myelinated axons, but there is no evidence for or against such a loss in relation to the degeneration of unmyelinated axons. Overall, however, Schwann cell numbers tend to increase as the number of myelinated axons increases.

Axons↗