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Biomedical subjects

D M Jacobson

Publications and source records attributed to D M Jacobson.

70 records · Page 4Linked to original sources
PubMed1989

Downbeat nystagmus associated with dolichoectasia of the vertebrobasilar artery.

We reviewed the case records and radiographic studies of 41 patients with primary position downbeat nystagmus seen during a 5-year period to investigate whether a relationship existed between dolichoectasia of the vertebrobasilar artery and cases of unknown cause. The cause of downbeat nystagmus could not be determined in 12 cases (29%). Two of these cases had dolichoectasia of the vertebrobasilar artery as the only identifiable abnormality. One other case had a dolichoectatic vertebrobasilar artery, but other potential etiologic factors for the development of downbeat nystagmus were present. Compression of the caudal brain stem by an enlarged and tortuous vertebrobasilar arterial system may be the cause of downbeat nystagmus in some cases unassociated with more commonly recognized causes.

Adolescent↗
PubMed1989

Amaurosis fugax associated with antiphospholipid antibodies.

In more than 50% of amaurosis fugax patients under 45 years of age no cause for the episodes of visual loss is identifiable. We have encountered 6 young adults (4 women and 2 men) with episodes of amaurosis fugax associated with elevated levels of antiphospholipid antibodies. Splinter hemorrhages of the nail beds were present in most patients. Treatment with antiplatelet medications and anticoagulants appeared to reduce the frequency of episodes and might prevent central retinal artery occlusions or stroke.

Adult↗
PubMed1989

X-linked progressive cone dystrophy. Clinical characteristics of affected males and female carriers.

The authors evaluated nine affected males and six female carriers from a four-generation family with X-linked cone dystrophy. As the affected males grew older, visual acuity deteriorated, central scotomas deepened, and macular changes became more prominent. There was granularity of the macula in younger individuals and bull's eye lesions and central geographic atrophy of the retinal pigment epithelium (RPE) in the older subjects. The retinas of some affected males had a bronze-green tapetal-like sheen. Color vision was impaired in all affected males and resembled an acquired type II defect (Verriest classification). One younger subject had paradoxical pupillary constriction to darkness. Visual-evoked potential (VEP) latencies were prolonged in some affected males, suggesting that photoreceptor degeneration caused transsynaptic degeneration of ganglion cells. All female carriers had visual acuities of 20/30 or better, but some showed mild ophthalmoscopic changes and abnormalities of color vision, electroretinograms (ERGs), and VEPs.

Adolescent↗
PubMed1989

Downbeating nystagmus and other ocular motor defects caused by lithium toxicity.

We report the clinical and neuropathologic findings of a 63-year-old woman who died following an accidental lithium overdose that produced coma, respiratory depression, horizontal gaze palsy, and downbeating nystagmus. She also had mild hypomagnesemia. The pathology was cytotoxicity, predominantly in the regions of the nuclei prepositus hypoglossi and medial vestibular nucleus. Damage to this area with kainate and ibotenate in rhesus monkeys has produced horizontal gaze palsy and downbeating nystagmus. In addition, we report our clinical experience during the past 6 years with other examples of downbeating nystagmus in patients receiving lithium.

Cranial Nerve Diseases↗
PubMed1988

Maternal orbital hematoma associated with labor.

We examined two women with orbital hematomas that occurred during labor. Both women developed sudden diplopia, proptosis, and orbital pain. The location of the hematoma was confirmed by orbital echography and computed tomography. The patients were observed without surgical intervention. Neither patient developed clinical or echographic signs of compressive optic neuropathy. Clinical resolution occurred during the following two weeks. Serial standardized orbital echographic examinations documented resolution of the hematomas.

Adult↗
PubMed1988

Enlargement of the blind spot caused by papilledema.

Blind spot enlargement in papilledema has been attributed to either mechanical disruption of the integrity of the peripapillary percipient elements by the swollen optic disk or to the Stiles-Crawford effect. We investigated the possibility that blind spot enlargement in papilledema is caused, at least in part, by a refractive scotoma due to peripapillary hyperopia. We reduced the enlarged blind spot in a patient with focal peripapillary hyperopia, without papilledema, to near normal size by using progressively stronger plus lenses. Similarly, with the addition of plus sphere, we reduced the size of the blind spot in five of six patients with papilledema, but in none of our normal subjects.

Adult↗
PubMed1988

Optic neuritis in the elderly: prognosis for visual recovery and long-term follow-up.

We evaluated 14 patients with idiopathic optic neuritis, 50 years of age or older, within 1 month of symptomatic onset from 1980 through 1985. We obtained follow-up information from case records an average of 13 months after initial examination and from telephone interviews an average of 57 months after initial evaluation. Four patients were men and ten were women. Visual loss was monocular in ten cases and binocular in four. Only one of 18 affected eyes initially had an acuity of 20/30 or better. Eleven eyes recovered acuities of 20/30 or better. There was no apparent benefit to those patients treated with corticosteroid agents. Six patients (43%) developed other neurologic sequelae an average of 16 months later; four (28%) had a second bout of optic neuritis and three (21%) developed clinically definite MS. Optic neuritis in the elderly behaves similarly to that disorder in younger age groups.

Aged↗
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↗
PubMed1987

Erythrocyte sedimentation rate and its relationship to hematocrit in giant cell arteritis.

We separated 24 patients with biopsy-proved giant cell arteritis into three groups based on erythrocyte sedimentation rates (ESRs) at clinical presentation: low, 1 to 40 mm/h; high, 41 to 80 mm/h; and very high, greater than 80 mm/h. The presence of anemia in the very high ESR group compared with the low ESR group was the only statistically identified difference. A linear regression analysis confirmed a high degree of inverse correlation between ESR and hematocrit in the subject population. There was no difference in ischemic ocular complications among the three groups. These findings emphasize that the diagnosis of giant cell arteritis should be made predominantly on clinical suspicion with less reliance on the ESR as a diagnostic criterion. Furthermore, the degree of ESR elevation does not predict which patients are at increased risk for the development of ocular complications. Finally, the ESR may not reliably indicate active disease in patients with normal hematocrit values.

Blood Sedimentation↗
PubMed1986

The neurologic manifestations of fat embolism.

We reviewed the clinical features of 12 patients with fat embolism seen in 10 years. Based on neurologic manifestations, patients were grouped into those with focal cerebral syndromes and those with diffuse encephalopathy. Patients with focal signs tended to present earlier with neurologic findings alone, did not have fever, and had less risk of pulmonary disorder than patients with encephalopathy.

Adult↗
PubMedDate not supplied

Systemic cholesterol microembolization syndrome masquerading as giant cell arteritis.

Two patients with clinical features consistent with giant cell arteritis were found to have systemic cholesterol microembolization syndromes. Diagnostic confirmation was established by a muscle biopsy in one patient and by a kidney biopsy in the other. Systemic cholesterol embolization can masquerade as a variety of disorders, including vasculitis, and should be considered in a patient with suspected giant cell arteritis who has a negative temporal artery biopsy.

Aged↗
PubMedDate not supplied

Recurrent cerebral infarctions in two brothers with antiphospholipid antibodies that block coagulation reactions.

Inhibitors blocking coagulation reactions, often called lupus anticoagulants, are readily identifiable but rarely considered as risk factors for cerebral infarction. These inhibitors are inconsistently found in a number of diseases (often autoimmune) and after treatment with ceretain drugs and appear to be closely associated with, or identical to, antibodies to certain phospholipids. We have observed two brothers with these inhibitors who both experienced recurrent cerebral infarctions. Such familial occurrence has rarely been reported. In addition, some other family members were found to have depressed factor XII levels. Using the technique of double immunodiffusion, we found that the serum from these brothers formed precipitin lines against certain phospholipid substrates, lending further support to the antiphospholipid nature of this inhibitor.

Adult↗
PubMedDate not supplied

Lupus anticoagulant.

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Blood Coagulation Disorders↗