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At least 109 records · Page 6Linked to original sources
PubMed2003

Incomitance of ocular rotation axes in trochlear nerve palsy.

Strabismus due to palsy of a single muscle in one eye is always incomitant, which is a consequence of Hering's law of equal innervation. We asked whether this law had similar consequences on the orientation of ocular rotation axes. Patients with unilateral trochlear nerve palsy were oscillated about the nasooccipital (= roll) axis (+/-35 degrees, 0.3 Hz), and monocularly fixed on targets on a head-fixed Hess screen. Both the covered and uncovered eyes were measured with dual search coils. The rotation axis of the covered eye (paretic or healthy) tilted more nasally from the line of sight when gaze was directed toward the side of the healthy eye. The rotation axis of the viewing eye (paretic or healthy), however, remained roughly aligned with the line of sight. We conclude that incomitance due to eye muscle palsy extends to ocular rotation axes during vestibular stimulation.

Adolescent↗
PubMed1999

Trochlear nerve.

Explore the source record for details and available documents.

Humans↗
PubMed2003

Primary position and listing's law in acquired and congenital trochlear nerve palsy.

PURPOSE: In ocular kinematics, the primary position (PP) of the eye is defined by the position from which movements do not induce ocular rotations around the line of sight (Helmholtz). PP is mathematically linked to the orientation of Listing's plane. This study was conducted to determine whether PP is affected differently in patients with clinically diagnosed congenital (conTNP) and acquired (acqTNP) trochlear nerve palsy. METHODS: Patients with unilateral conTNP (n = 25) and acqTNP (n = 9) performed a modified Hess screen test. Three-dimensional eye positions were recorded with dual search coils. RESULTS: PP in eyes with acqTNP was significantly more temporal (mean: 21.2 degrees ) than in eyes with conTNP (6.8 degrees ) or healthy eyes (7.2 degrees ). In the pooled data of all patients, the horizontal location of PP significantly correlated with vertical noncomitance with the paretic eye in adduction (R = 0.59). Using a computer model, PP in acqTNP could be reproduced by a neural lesion of the superior oblique (SO) muscle. An additional simulated overaction of the inferior oblique (IO) muscle moved PP back to normal, as in conTNP. Lengthening the SO and shortening the IO muscles could also simulate PP in conTNP. CONCLUSIONS: The temporal displacement of PP in acqTNP is a direct consequence of the reduced force of the SO muscle. The reversal of this temporal displacement of PP, which occurs in some patients with conTNP, can be explained by a secondary overaction of the IO muscle. Alternatively, length changes in the SO and IO muscles, or other anatomic anomalies within the orbit, without a neural lesion, may also explain the difference in location of PP between conTNP and acqTNP.

Adaptation, Ocular↗
PubMed2005

[Head-tilt test in unilateral and symmetric bilateral acquired trochlear nerve palsy].

BACKGROUND: The head-tilt phenomenon (difference between the vertical deviations with an ipsilateral and contralateral head-tilt by 45 deg. each) occurring in patients with a superior oblique palsy has traditionally been explained by the lacking contraction of the superior oblique muscle within the synkinetic movement of ocular counterrolling. However, using a computer model, Robinson showed that the superior oblique palsy itself causes only a relatively small head-tilt phenomenon. Adaptive mechanisms amplifying the otolith reflex were suggested to explain the increase of the head-tilt phenomenon in the course of time. In order to reduce the abnormal head posture required for binocular vision, the otolith reflex would be amplified, accepting the greater vertical deviation when the head is tilted to the paretic side . QUESTION: If the head-tilt phenomenon were solely caused by the lacking contraction of the superior oblique muscle, it should be greater in bilateral than in unilateral superior oblique palsies. If an adaptive mechanism were acting to reduce the abnormal head posture, the head-tilt phenomenon should not be greater, and could even be smaller in bilateral than in unilateral superior oblique palsy, because in bilateral (symmetric) trochlear nerve palsies the vertical deviation at straight gaze is already small or absent without adaptation. PATIENTS AND METHODS: We have carried out a retrospective comparison of 10 patients with bilateral symmetric superior oblique palsies and 10 patients with unilateral superior oblique palsy. In all cases, the palsy was acquired and had been present for at least 1 year. RESULTS: The patients with bilateral superior oblique palsy had a head-tilt phenomenon ranging from 0 to 7 degrees (median, 2 deg.). The patients with unilateral superior oblique palsy had a head-tilt phenomenon between 2 and 13 degrees (median, 8 deg.). The difference was significant (p = 0.0117). CONCLUSIONS: The head-tilt phenomenon is smaller in long-standing bilateral symmetric superior oblique palsies than in long-standing unilateral superior oblique palsy. This finding supports the hypothesis that in unilateral superior oblique palsy, an adaptive mechanism augments the head-tilt phenomenon by an amplification of the otolith reflex. However, we presume that the amplification of the otolith reflex is only a side effect of the adaptive change of the vertical fusional vergence tonus and thus the price of the improved vertical fusion, rather than a compensatory mechanism.

Adaptation, Physiological↗
PubMed2006

Simultaneous, painless, homolateral oculomotor and trochlear nerve palsies in a patient with type 2 diabetes mellitus. Neuropathy or brainstem infarction?

Combined palsies of cranial nerves, especially of the oculomotor nerves, are distinctly uncommon, even in patients with diabetes mellitus. We present a patient with type 2 diabetes mellitus, arterial hypertension and hyperlipidaemia, who had simultaneous oculomotor and trochlear nerve palsies. An MRI scan showed multiple brainstem ischaemic infarcts. The patient was treated with intensified insulin regimen and clopidogrel. Symptoms gradually improved, and at 9 months there was no further improvement.

Aged↗
PubMed1990

Regeneration and soma size changes following axotomy of the trochlear nerve.

The effects of CNS and PNS axotomy of the IVth nerve on cell death, soma size, axon size, and axon number were investigated. In adult cats, the IVth nerve was axotomised by using four surgical paradigms: (1) peripheral IVth nerve crush, (2) peripheral IVth nerve cut, (3) peripheral IVth nerve resection, and (4) a CNS IVth nerve cut in the velum. The extent of cell death resulting from each surgical paradigm was determined. Following axotomy distal to the decussation of the IVth nerves, cell death was least after nerve crush, intermediate after nerve cut, and maximal after resection of 5-7 mm of the nerve. Following axotomy at the decussation--a CNS lesion--most cells died but some successful regeneration was observed. Soma size measurements following a short-term survival (3 days to 4 weeks) before the regenerating axons reached their target muscle revealed that somas of axotomised cells underwent hypotrophy within 1 week of axotomy and then gradually increased in size. They re-attained normal size by 4 weeks postoperative when regenerating axons first reach their target. Following a long-term survival (greater than 2 months), somas were significantly hypertrophied, and the degree of hypertrophy was inversely related to the extent of cell survival up to a limit of 40% soma size increase. Counts and measurements of axons revealed that mean axon diameter of regenerated axons was much smaller than normal 3 months after axotomy, increased during the third to sixth postoperative months, but then showed no subsequent increase and remained below normal. In animals with cell death varying from 10% to 70%, the number of axons in the nerve was maintained constant at approximately 1,000. These data indicate that there is a mechanism for the production and maintenance of the appropriate number of regenerative axonal branches following axotomy. In animals in which cell death exceeded 70%, the number of axons was controlled by a maximum ratio of 3 to 4 axon branches per surviving cell. The results suggest that axon number is strongly influenced by the target muscle and that hypertrophy of regenerated cells is related to the number of axonal sprouts each cell has to produce and support in order to re-establish the preoperative number of axons in the regenerated trochlear nerve.

Animals↗
PubMed1986

[Medical findings on the trochlear nerve].

The exit-zone, the intracisternal course, the course in the sidewall of the cavernous sinus and inside the orbit were measured at 91 head-halves. Included are measurements of the length of the area nervosa, its nerve fibers and its distance to the total extracerebral length of the IVth nerve is estimated. The results are discussed with earlier investigations and some clinical approaches and neurophysiological methods are given.

Adult↗
PubMed1979

The growth and development of the superior oblique muscle and trochlear nerve in juvenile and adult goldfish.

Superior oblique muscle/trochlear nerve pairs from goldfish of various ages (1-5 years) have been examined light and electron microscopically. The muscle grows by enlargement (longitudinally and transversely) of individual fibers, and by addition of new ones at the rate of about 250/year. The nerve grows by enlargement of fibers, but few and perhaps no new axons are added. The somata enlarge, and the neuromuscular synapses become much more numerous. The ratio of muscle fibers to nerve fibers increases from about 5 in the young to about 16 in the old fish.

Animals↗
PubMed1990

The effects of intrauterine growth retardation on the structural development of cranial nerves (optic, trochlear) in fetal sheep.

A quantitative morphometric study of the development of myelinated fibres in the optic and trochlear nerves has been made in growth-retarded fetal sheep at 140 days gestation (term = 146 days). Intrauterine growth retardation was induced as a result of the reduction of placental mass, by prior removal of placentation sites in six ewes. In the optic nerve (central nervous system) the mean diameter of myelinated fibres was not significantly reduced but the thickness of the myelin sheath relative to axon diameter was disproportionately reduced. In the trochlear nerve (peripheral nervous system) there was a significant reduction of 23% (P less than 0.01) in the mean diameter of myelinated fibres; however the normal axon:myelin ratio was maintained. The total number of myelinated fibres in the trochlear nerve did not differ between the normal and growth-retarded group, indicating that there was not a greater than normal incidence of cell death during intrauterine growth retardation in the nucleus of the trochlear nerve. The differential effect of intrauterine growth retardation on myelination in the central and peripheral nervous systems suggests that chronic intrauterine deprivation affects oligodendrocyte activity but does not markedly affect the capacity of Schwann cells to produce myelin.

Animals↗
PubMed1986

Traumatic trochlear-nerve palsy due to haematoma.

An unusual case is described of traumatic fourth cranial-nerve palsy due to a small haematoma in the region of the superior cerebellar cistern. The clinical picture improved with resorption of the haematoma.

Cerebellum↗