PubMed Health⌕ Search

Biomedical subjects

Jonathan D Trobe

Publications and source records attributed to Jonathan D Trobe.

At least 19 recordsLinked to original sources
PubMed2006

Third, fourth, and sixth cranial nerve palsies following closed head injury.

BACKGROUND: The relationship between the circumstances and severity of closed head injury (CHI) and the clinical and imaging features of cranial nerve 3, 4, and 6 palsies has not been rigorously addressed in a large study. METHODS: Retrospective chart review of 210 consecutive patients with CHI examined at a single tertiary care center from 1987 to 2002. Patients were located by searching the ophthalmology inpatient consultation and neuro-ophthalmology outpatient databases and hospital emergency room billing codes for a diagnosis of traumatic 3, 4, or 6 cranial nerve palsy (Cranial Nerve Injury Group) and a diagnosis of CHI without traumatic 3, 4, or 6 nerve palsy (Control Group). The Cranial Nerve Injury Group was then subdivided into two groups: those with injuries to an individual cranial nerve and those with multiple (including bilateral) cranial nerve injuries. Comparisons between groups were based on age, gender, type of accident, Glasgow Coma Scale (GCS), documented loss of consciousness (LOC), type of ocular injury, presence of systemic injury, need for rehabilitation, physical therapy and cognitive scores, and imaging features. RESULTS: The Cranial Nerve Injury Group had a significantly higher severity of head injury, more CT abnormalities, and worse short-term neurologic outcomes as compared with the Control Group. These trends were also found when each cranial nerve injury subgroup was compared with the Control Group. Those with cranial nerve 3 palsy had the most severe head injury; those with cranial nerve 4 palsy had an intermediate level of head injury; and those with cranial nerve 6 palsy had the lowest level of head injury. There were no consistent associations between the location of the imaging abnormalities and which cranial nerve was damaged. CONCLUSIONS: CHI with palsy of an ocular motor nerve was more severe than CHI without ocular motor nerve palsy, as measured by the GCS, intracranial and skull imaging abnormalities, and a greater frequency of inpatient rehabilitation. Palsy of cranial nerve 3 was associated with relatively more severe CHI than was palsy of cranial nerves 4 or 6. The location of the imaging abnormalities did not correlate with a particular cranial nerve injury.

Abducens Nerve Diseases↗
PubMed2006

Pitfalls in the diagnosis of mitochondrial encephalopathy with lactic acidosis and stroke-like episodes.

We describe a patient with genetically- and biochemically-proven mitochondrial encephalopathy with lactic acidosis and stroke-like episodes (MELAS) who was initially misdiagnosed as having had multiple ischemic strokes in part because the clinical presentation appeared to be acute, the MRI of lesions showed restricted diffusion, and the brain biopsy showed features suggestive of stroke. This report emphasizes the pitfalls in the diagnosis of MELAS and points out the similarities and differences between MELAS and ischemic stroke.

Acidosis, Lactic↗
PubMed2006

Multiple brain infarcts and Balint syndrome in aortic arch angiosarcoma.

A 50-year-old woman presented with subacute cognitive decline, impaired eye movements, and simultanagnosia, components of the Balint syndrome. She had relatively low blood pressure in the left arm and left finger clubbing. Brain imaging identified multiple acute infarcts. Transesophageal echocardiography showed no cardiac abnormalities but demonstrated a thickened aortic wall and an intraluminal aortic arch mass. The surgical specimen revealed angiosarcoma. Of the few reported angiosarcomas involving the aorta, most have been located in the abdominal segment. This is only the second reported case of aortic arch sarcoma presenting with stroke.

Agnosia↗
PubMed2006

Papilledema in the assessment of ventriculomegaly.

To determine whether ventriculomegaly is associated with ongoing increased intracranial pressure (ICP), physicians often rely on corroborative imaging features such as altered periependymal signal, distortion of ventricular shape, subarachnoid space flattening, and an increase in ventricular size over time. In 2 patients with new headache and altered mental status, symptoms and ventriculomegaly were dismissed as long-standing and not reflective of current ICP elevation. In the first patient, ICP was considered normal because there were no corroborative imaging features of elevated ICP. In the second patient, ICP was considered normal because ventricular size was stable over a 1-year period. The diagnosis of ICP elevation was finally made by ICP monitoring after papilledema was recognized. Ventriculoperitoneal shunting rapidly resolved the papilledema and markedly improved mentation. Brain imaging may often be an unreliable guide to the presence of elevated ICP. In such patients, the finding of papilledema is a critical determinant of management.

Adult↗
PubMed2005

Transient monocular visual loss.

PURPOSE: To provide a practical update on the diagnosis and management of transient monocular visual loss (TMVL). DESIGN: Perspective. METHODS: Review of the literature. RESULTS: TMVL is an important clinical symptom. It has numerous causes but most often results from transient retinal ischemia. It may herald permanent visual loss or a devastating stroke, and patients with TMVL should be evaluated urgently. A practical approach to the evaluation of the patient with TMVL must be based on the patient's age and the suspected underlying etiology. In the older patient, tests should be performed to investigate giant cell arteritis, atherosclerotic large vessel disease, and cardiac abnormalities. In the younger patient, TMVL is usually benign and the evaluation should be tailored to the particular clinical setting. CONCLUSIONS: Specific prevention strategies are tailored to the most likely cause of TMVL and the patient's underlying risk factors. Prevention of a future event should begin in the ophthalmologist's office with education and aggressive treatment of artherosclerotic risk factors.

Humans↗
PubMed2005

Homonymous hemianopia caused by occipital lobe infarction in heparin-induced thrombocytopenia and thrombosis syndrome.

A 73-year-old woman developed mental confusion and finger pain after treatment with enoxaparin following arthroplasty. A platelet count was 163,000/microL. Because digital embolism was suspected, she was emergently treated with heparin and recombinant tissue plasminogen activator (rTPA). During rTPA infusion, she reported sudden hemifield loss, so the infusion was aborted. Brain CT disclosed a non-hemorrhagic occipital infarct. Platelets had fallen to 63,000 over eight days, and antibodies against a complex of heparin and platelet factor 4 were detected. These findings led to the diagnosis of heparin-induced thrombocytopenia and thrombosis syndrome (HITTS), an immune-mediated disorder in which venous and arterial thromboses occur. Right lower extremity deep venous thromboses were later diagnosed, and an MRI disclosed multiple cerebral infarcts of recent onset but different ages. Previous reports have documented brain arterial strokes in HITTS, mostly in the distribution of the middle cerebral artery, but clinical documentation is sparse, and there have been no imaging reports. This is the first report to document the clinical and imaging features of a HITTS stroke and the first to describe a stroke presumptively caused by a low molecular weight heparin. It emphasizes that HITTS may cause stroke even when the platelet count is normal. Diagnosis of HITTS should prompt immediate cessation of heparin treatment and substitution of a direct thrombin inhibitor or fondaparinux.

Aged↗
PubMed2005

Ocular ischemic syndrome after occlusion of both external carotid arteries.

The ocular ischemic syndrome (OIS) has been reported in association with high-grade stenosis or occlusion of the common carotid artery (CCA) or internal carotid artery (ICA) but never with high-grade stenosis or occlusion of the external carotid artery (ECA) alone. We describe two patients who developed OIS with bilateral occlusion of the ECAs yet patent CCAs and ICAs. In one case, unilateral OIS followed consecutive bilateral carotid endarterectomies. In the other case, OIS developed spontaneously OU but was exacerbated in one eye after ipsilateral carotid endarterectomy (CE) in the setting of pre-existing contralateral ECA occlusion. In some individuals, the ECA is the primary source of arterial blood flow to the eye. Because of this fact, the endarterectomy surgeon must avoid causing ECA occlusion by meticulously removing not only the ICA plaque, but also the entire ECA plaque.

Aged↗
PubMed2004

Neurologic impairment 10 years after optic neuritis.

BACKGROUND: Participants enrolled in the Optic Neuritis Treatment Trial have been observed for more than a decade to assess the relationship between optic neuritis and the development of clinically definite multiple sclerosis. OBJECTIVE: To assess neurologic disability 10 to 12 years after an initial episode of optic neuritis. DESIGN: Longitudinal follow-up of a clinical trial. SETTING: Fourteen Optic Neuritis Treatment Trial clinical centers performed standardized neurologic examinations, including an assessment of neurologic disability. PARTICIPANTS: One hundred twenty-seven patients who had developed clinically definite multiple sclerosis. MAIN OUTCOME MEASURES: Functional Systems Scale and Expanded Disability Status Scale. RESULTS: The disability of most patients was mild, with 65% of patients having an Expanded Disability Status Scale score lower than 3.0. The degree of disability appeared to be unrelated to whether the baseline magnetic resonance imaging scan was lesion-free or showed lesions (P =.51). Among patients with baseline lesions, the degree of disability was unrelated to the number of lesions that were present on the scan (P =.14). Two patients died owing to severe multiple sclerosis, one of whom had no lesions revealed on the baseline scan. CONCLUSION: Most patients who develop clinically definite multiple sclerosis following an initial episode of optic neuritis will have a relatively benign course for at least 10 years.

Adult↗
PubMed2004

Visual function more than 10 years after optic neuritis: experience of the optic neuritis treatment trial.

PURPOSE: To assess visual function more than 10 years after an episode of optic neuritis in patients enrolled in the Optic Neuritis Treatment Trial. DESIGN: Longitudinal follow-up of a randomized clinical trial. METHODS: Vision testing included measures of visual acuity, contrast sensitivity, and visual field. Quality of life was assessed with the National Eye Institute Visual Function Questionnaire. RESULTS: Examinations were completed on 319 patients. In most patients, visual function test results in the eyes that experienced optic neuritis at study entry ("affected eyes") were normal or only slightly abnormal after 9.9 to 13.7 years. Visual acuity in the affected eyes was >or=20/20 in 74%, 20/25 to 20/40 in 18%, <20/40 to 20/200 in 5%, and <20/200 in 3%. On average, visual function was worse in patients with multiple sclerosis (MS) than in those without MS. Recurrent optic neuritis in either eye occurred in 35% of patients. Such attacks were more frequent in patients with MS (P <.001). The National Eye Institute Visual Function Questionnaire scores were lower when visual acuity was abnormal and when MS was present. CONCLUSIONS: Most patients retained good to excellent vision more than 10 years after an attack of optic neuritis. Recurrences were more frequent in patients with MS.

Adolescent↗
PubMed2004

Facial and trigeminal neuropathies in cavernous sinus fistulas.

Three patients with carotid-cavernous fistulas had prominent ipsilateral facial nerve neuropathy. One patient also had ipsilateral third division trigeminal neuropathy, manifesting as painful trismus and lower facial numbness. Rarely reported in carotid-cavernous fistula, these neuropathies may occur when there is substantial drainage of the fistula into a dilated inferior petrosal sinus. Closure of the fistula in two cases resulted in full recovery of the neuropathies within weeks to months. The neuropathies may be caused by ischemia from an unfavorable arteriovenous flow gradient, venous compression, or secondary inflammation.

Adult↗
PubMed2004

Metastatic neuroblastoma presenting with binocular blindness from intracranial compression of the optic nerves.

A 2-year-old boy with blindness as an isolated symptom was found to have no light perception binocularly because of compression of both optic nerves by a neuroblastoma infiltrating the walls of the optic canals and medial sphenoid bone. Imaging disclosed a primary tumor near the kidney and multiple osseous metastases. Although neuroblastoma commonly causes blindness by metastasis to the orbit, it rarely causes bilateral blindness from intracranial compression of the optic nerves. This is the first report of bilateral blindness as the presenting feature.

Blindness↗
PubMed2004

Galloping ophthalmoplegia and numb chin in Burkitt lymphoma.

A 57-year-old man developed complete bilateral ophthalmoplegia over a period of 10 days, together with bilateral facial pain and numbness of the chin. He had no other clinical manifestations. Findings on brain magnetic resonance imaging and spinal fluid formula from the first lumbar puncture were normal, but cerebrospinal fluid flow cytometry disclosed a kappa restriction monoclonal B-cell population, indicating malignant lymphoma. Computed tomography of the chest, abdomen, and pelvis then revealed multiple enlarged lymph nodes. Biopsy of an inguinal node showed findings consistent with Burkitt lymphoma. Within six weeks, intravenous and intrathecal chemotherapy resolved all neurologic findings except a partial right-side sixth nerve palsy and mild chin numbness. Eighteen months after disease onset, the patient remained in remission. Meningeal spread of Burkitt lymphoma is not commonly a presenting feature in immunocompetent adults. Chin numbness, a characteristic feature caused by infiltration of the mental nerve, should facilitate earlier recognition, which may be life saving.

Antimetabolites, Antineoplastic↗
PubMed2004

Ophthalmic artery occlusion secondary to radiation-induced vasculopathy.

A 35-year-old man with neurofibromatosis type 1 (NF1) had a left ophthalmic artery occlusion that caused no light perception OS 28 years after having been treated with external beam radiation therapy for a presumed glioma of the right optic nerve and chiasm. Clinical and imaging findings were consistent with radiation-induced cerebral vasculopathy. This ophthalmic complication has never been reported, despite the common occurrence of severe carotid-ophthalmic artery junction stenosis after radiation in NF1 patients. Even though modern radiation techniques limit collateral damage, this modality should be used with discretion in NF1 patients, given the vulnerability of their immature cerebral vasculature to radiation.

Adult↗
PubMed2004

Magnetic resonance imaging of suspected cervicocranial arterial dissections.

The authors propose that the optimal screening protocol for evaluation of suspected cervicocranial arterial dissections is magnetic resonance imaging (MRI) that includes three components: 1) contrast-enhanced three-dimensional time-of-flight magnetic resonance angiography (MRA) through the superior mediastinum, neck, and skull base; 2) three-dimensional multiple overlapping thin-section acquisition MRA of the skull base and Circle of Willis region; and 3) axial non-contrast, non-fat-suppressed T1-weighted, fat-suppressed T1-weighted, and T2-weighted spin-echo MRI from the level of the aortic arch through the level of the circle of Willis. MRA permits visualization of vascular luminal narrowing or obliteration, which can suggest vascular dissection but can also be caused by congenital variation, dysplasia, intraluminal thrombus, vasospasm, or extramural compression by tumor. By directly visualizing the blood vessel wall, axial T1-weighted and T2-weighted spin-echo MRI can identify the intramural hemorrhage of vascular dissection. This protocol is designed to maximize the sensitivity of a noninvasive technique and may eliminate the need for conventional endovascular angiography.

Adult↗
PubMed2003

High- and low-risk profiles for the development of multiple sclerosis within 10 years after optic neuritis: experience of the optic neuritis treatment trial.

OBJECTIVE: To identify factors associated with a high and low risk of developing multiple sclerosis after an initial episode of optic neuritis. METHODS: Three hundred eighty-eight patients who experienced acute optic neuritis between July 1, 1988, and June 30, 1991, were followed up prospectively for the development of multiple sclerosis. Consenting patients were reassessed after 10 to 13 years. RESULTS: The 10-year risk of multiple sclerosis was 38% (95% confidence interval, 33%-43%). Patients (160) who had 1 or more typical lesions on the baseline magnetic resonance imaging (MRI) scan of the brain had a 56% risk; those with no lesions (191) had a 22% risk (P<.001, log rank test). Among the patients who had no lesions on MRI, male gender and optic disc swelling were associated with a lower risk of multiple sclerosis, as was the presence of the following atypical features for optic neuritis: no light perception vision; absence of pain; and ophthalmoscopic findings of severe optic disc edema, peripapillary hemorrhages, or retinal exudates. CONCLUSIONS: The 10-year risk of multiple sclerosis following an initial episode of acute optic neuritis is significantly higher if there is a single brain MRI lesion; higher numbers of lesions do not appreciably increase that risk. However, even when brain lesions are seen on MRI, more than 40% of the patients will not develop clinical multiple sclerosis after 10 years. In the absence of MRI lesions, certain demographic and clinical features seem to predict a very low likelihood of developing multiple sclerosis. This natural history information is a critical input for estimating a patient's 10-year multiple sclerosis risk and for weighing the benefit of initiating prophylactic treatment at the time of optic neuritis or other initial demyelinating events in the central nervous system.

Acute Disease↗