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Results for “OCULOMOTOR PARALYSIS”

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At least 19 recordsLinked to original sources
PubMed1981

Transient oculomotor paralysis in pseudotumor cerebri.

Transient oculomotor paralysis developed abruptly in a patient with well-documented pseudotumor cerebri. Other demonstrable causes of third-nerve palsy were excluded. Sixth-nerve palsy is known to occur in 10 to 40% of patients in most series of pseudotumor cerebri, but third-nerve palsy has not been reported previously. It may also be a nonspecific sign of raised intracranial pressure.

Adult↗
PubMed1978

Isolated oculomotor paralysis. The product of saccular and fusiform aneurysms of the basilar artery.

Isolated oculomotor paralysis was produced by an unsuspected saccular basilar aneurysm in one case and fusiform basilar aneurysm in another. The chronicity of symptoms and lack of pain were misleading features. The saccular basilar aneurysm, which has an untreated mortality of 50% to 80%, was visualized best with selective angiography and successfully clipped intracranially. The fusiform basilar aneurysm, part of a diffuse atherosclerotic ectasia of all basal intracranial arteries, indented and displaced the upper brain stem. A common ophthalmologic sign of posterior communicating aneurysms, oculomotor paralysis has not been documented frequently with basilar aneurysms.

Aneurysm↗
PubMed2002

[A patient with primary Sjögren's syndrome featuring polyneuropathy and oculomotor paralysis and associated with asymptomatic left middle cerebral artery stenosis].

We report a case of primary Sjögren's syndrome (primary SjS) with polyneuropathy and right oculomotor paralysis associated with middle cerebral artery stenosis. A 39-year-old woman developed progressive numbness and clumsiness of the limbs. Two months later, right third cranial palsy manifested itself and she was admitted to our hospital. A cranial MRA showed left middle cerebral artery stenosis confirmed by transcranial color doppler sonography. A nerve conduction study showed a decrease in the NCV and reduced CMAP, while sural nerve biopsy showed axonal degeneration and infiltration of inflammatory cells around the small blood vessel walls. The patient complained of dry mouth and a salivary gland biopsy revealed inflammatory changes, while salivary gland scintigraphy showed diminished secretion. These findings led to the diagnosis of Sjögren's syndrome. Reports of primary SjS with involvement of large cerebral arteries are rare. In our case, polyneuropathy and oculomotor paralysis were the manifest symptoms, but middle cerebral artery stenosis was also observed. This indicates that, even in the absence of CNS symptoms, cerebral artery involvement may be present in primary SjS.

Adult↗
PubMedDate not supplied

[Etiologic diagnosis of oculomotor paralysis by computerized tomography: a statistical approach. Apropos of 472 cases].

Among 4,538 neuroradiology cases gathered at the NOHC of the XV-XX, an oculomotor paralysis is the 3rd (37.65%) clinical circumstances justifying a computerized tomography (directional plane by the neuro-ocular plane or PNO). The interpretation of the investigations requires to index them in 7 groups of items, therefore a computerized access follows (cross-sorting data). The injury of the VI overcomes (39.61%) followed by the one of the III (33.68%), and the IV (6.35%). In spite of limitations, the study puts forward and debates about etiological frequencies sometimes different from those in the literature.

Adolescent↗
PubMed1989

[Herpes zoster ophthalmicus with subsequent oculomotor paralysis and homolateral media infarct].

Oculomotor palsy is a well-known complication of herpes zoster ophthalmicus (HZO). Combination with homolateral cerebral media infarction and contralateral hemiplegia is very rare. Since the first paper on HZO and cerebral ischemia was published, in 1919, about 70 cases have been described. Zoster infection is thought to encroach from the fifth cranial nerve on to a cerebral artery at the base of the brain. The authors describe a case of HZO seen by them, with oculomotor palsy and ipsilateral media infarction with contralateral hemiplegia and aphasia. A review of the literature is given and etiologic and therapeutic aspects are discussed.

Aphasia↗
PubMed1990

[Oculomotor paralysis caused by lesion of the brain stem].

Oculomotor palsies due to lesions of the brain stem may be complete, affecting all types of eye movements in one direction; this reflects a nuclear, internuclear or infractuclear lesion. This may also be disassociated, affecting only one type of eye movements, and this suggests supranuclear lesions. Concerting lateral movements, complete paralysis of abduction, adduction (sparing convergence) or ipsilateral laterality is suggestive of damage to the radicular fibres of the abducencs nucleus (VI), to its internuclear neurons or to the nucleus itself respectively. Isolated paralysis of saccades is in favour of a lesion of the paramedian pontine reticular formation. As regards vertical movements, paralysis of the oculomotor nerve (III), either isolated or associated with complete paralysis of the contralateral rectus superior oculi muscle, suggests a lesion of the radicular fibres of III or of the nucleus itself respectively. Paralysis of downward or both downward and upward saccades indicates the presence of bilateral lesions in the region of the mesencephalic reticular formation. Paralysis of upward saccades alone reflects a unilateral lesion located near the posterior commissure.

Brain Stem↗
PubMedDate not supplied

[Acquired oculomotor paralysis in the adolescent].

INTRODUCTION: Acquired oculomotor palsy in juvenile age are most commonly due to head trauma, tumors, migraine, vasculopathies and demyelinating diseases. CLINICAL CASES: We document three cases of paroxysmal oculomotor nerve palsy in childhood, illustrating the main clinical symptoms, neurological examination, MR images, diagnosis, treatment and evolution. Final diagnosis were: multiple sclerosis, pineoblastoma, and craniopharyngioma. CONCLUSIONS: Sudden oculomotor nerve palsy occurring in youth in the absence of head trauma, viral infection or migraine access, firmly suggests a serious intracranial disease, and neuroimage studies should be quickly obtained to have an early diagnosis.

Adolescent↗
PubMed1984

[Isolated oculomotor paralysis in the aged].

Six patients aged between 57 and 78 years suddenly developped an oculomotor nerve paralysis without other ocular lesions, but with evidence of arterial hypertension of probable etiological significance. Recovery was complete in all cases.

Age Factors↗